Scottish Doctor, author, speaker, sceptic

Cholesterol lowering – the end of the beginning?

I have been somewhat silent over the last two or three weeks on this blog. The word ‘swamped’ springs to mind. The main swamping thing (alongside work and suchlike) that I have been doing is to analyse the Lancet paper which claimed that, basically, statins cause no adverse events. Professor Peter Sever (corresponding author), followed up the publication of this paper with statements such as:

And so on and so forth. This paper, as you may expect, has been picked up with great enthusiasm by the mainstream medical media, and other doctors. Here is a Dr John Mandrola writing a Commentary in Medscape.

As a practicing doctor, I have always felt the truth lies closer to the observational data. A study published recently in the Lancet suggests I may be wrong. This new study, which has impeccable methods, suggests statin muscle complaints stem not from human muscles but from the human brain. In the Lancet paper, researchers took advantage of two distinct parts of the primary prevention ASCOT-LLA trial.

In the first part of ASCOT-LLA, more than 10,000 people were randomized to either atorvastatin 10 mg daily or placebo in a double-blinded fashion. After completion of the blinded phase of ASCOT-LLA, study participants were invited to take part in a nonblinded and nonrandomized extension study in which they could take atorvastatin open label.

The results turned on whether people knew they were on the statin. In the double-blinded phase of the trial, muscle symptoms occurred at the same rate—2.0% per year in both the statin and placebo groups. In the second phase of the trial, when people knew they were on the statin, side effects occurred at a higher rate (1.3% per year) in the statin group vs the placebo group (1.0% per year). This difference reached statistical significance (hazard ratio 1.41, CI 1.10–1.79; P=0.006).

These are remarkable observations, which are hard to dispute. In an accompanying editorial, two Spanish authors emphasized the obvious strengths of this paper: these were the same patients in both phases, and there was no run-in period in which patients intolerant to statins were excluded’ (http://www.medscape.com/viewarticle/879762_print).

So, this is a slam dunk. Right?

Well, I have taking a pretty forensic look at the Lancet Paper. It has the snappy title. ‘Adverse events associated with unblinded, but not with blinded, statin therapy in the Angle-Scandinavian Cardiac Outcomes Trial – Lipid Lowering Arm (ASCOT-LLA); a randomised double-blind placebo-controlled trial and its non-randomised non-blind extension phase.’ May 2nd 2017’.

You may not be surprised to know that Professor Sir Rory Collins was a co-author.

I believe it may have a weakness – or two – or three – or … you get the picture. However, if you are going to attempt to argue against such a paper, or pick holes in it, you need to study it with extreme care, to make sure that you have your facts absolutely right.

Then you need to look at all other associated papers around the entire ASCOT study. For example, I have been amusing myself, or not, by studying ‘Rationale, design, methods and baseline demography of participants in the Anglo-Scandinavian Cardiac Outcomes Trial’…. And a few other papers as well. I have also been speaking to some very bright people who understand exactly how clinical studies are done, how adverse events are reported and recorded. It is an arcane and opaque world indeed.

You need to try to understand comments such as this, in the paper:

Procedures

‘After randomisation, study participants were scheduled to be seen at 6 weeks and 3 months and then at 6 monthly intervals thereafter during both the blinding randomised and non-blinding randomised phases of the ASCOT-LLA (until the ASCOT-BPLA completed – yes this was two trials in one). At each study visit all adverse events (AEs) reported by participants were recorded by the study team in the case report form. Specific questions relating to any putative AEs were not asked at these visits.

Reports of AEs by the study participants were initially recorded verbatim and subsequently classified with use of the Medical Dictionary for Regulatory Activities into 26 separate system organ class (SOC) groups, 2288 unique preferred terms, and 5109 separated low-level terms…..’

Now, I defy anyone to make sense of that. [I had no idea what the word putative meant in this context. Having looked it up, I am none the wiser]. Either adverse reports were initially recorded onto a case report form, or comments were recorded verbatim and subsequently classified…. You can do one, or the other, not both. As for attempting to reclassify verbatim reports, in several different languages, fifteen years later…. Hmmmmm.

However, whilst trying to get my head around that, my interest was piqued by those involved in this data analysis. It turns out that the lead author, Ajay Gupta, was provided with financial support from the ‘Foundation for Circulatory Health’. I had never heart of this ‘charity’ before. So I tried to find out how it was funded – always tricky. You can usually find out who provides the dosh, but not how much.

Looking at their accounts, the foundation for Circulatory Health seems to be funded largely (almost entirely?) by the pharmaceutical industry. Companies which include, guess who, Pfizer, who funded the initial ASCOT study and who also funded the recent Lancet Nocebo paper.

Digging further it then turned out that that Peter Sever and Neil Poulter (key authors on the ‘nocebo’ paper) are also directors of the Foundation for Circulatory Health, which Funded Dr Gupta to work on the Nocebo paper – supported by Pfizer. Well, who’d a thunk? [Well, me actually].

Neil Poulter is a very well-known researcher in CV medicine, well known to those who keep track of such things. His name turns up all over the place. Here was his declaration of interest statement in the Lancet paper:

‘Neil Poulter’s institution (Imperial College London) held a grant for the conduct of the Anglo-Scandinavian Cardiac Outcomes Trial in the UK and Ireland and he has also received a speaker’s honoraria from Pfizer outside the submitted work. He is also a recipient of the National Institute for Health Research Senior Investigator Award to Imperial College Healthcare NHS Trust.’

Sounds quite reasonable(ish) and above board. However, compare this with a conflict of interest statement from 2008: ‘Poulter disclosed receiving ad hoc payments to appear on advisory boards/deliver lectures for “all the major pharmaceutical companies that produce major agents in hypertension and CV medicine” and receiving grant income from Pfizer and Servier’(http://www.medscape.com/viewarticle/790044?t=1#vp_2).

Perhaps he just forgot that he had received money from all the major pharmaceutical companies that produce major agents in hypertension and CV medicine. Must be hard to keep track of what you have previously disclosed. Is there a time limit on conflicts of interest?

For now, I shall continue to dig. I shall continue to analyse the paper. Watch this space. It is all rather time consuming, but it may turn out rather well in the end. Although, I suppose, that rather depends on which side you are on in this debate.

312 thoughts on “Cholesterol lowering – the end of the beginning?”

Thank you for all the time you take looking into this stuff for us. I hope you still have time to relax! There must be a lot of ‘experts’ groaning when they know you’ve been looking into what they do again. They must wish you would retire – or worse! At least if anything nasty happened to you there would be a long list of Suspects. And their names are all here in your blog! You’ are a brave wee mon – as my granny would say. Thank you again. I think a lot of us would say you are our hero?
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I was thinking the same thing, Sue! I’ll bet all those “expert doods” start thinking “Oh no, here comes that Kendrick guy again and we’re all gonna hafta explain our non-sequitur answers at some point”. Too funny!

Yes, thank you Dr. Kendrick for doing all the leg work on these issues. I always appreciate your opinions and logic, compared to the twaddle we get from these mostly bogus “studies”. I really don’t know how they can even call them studies OR scientific when they are so biased, but money talks, doesn’t it?

I am a lay person, but from a medical family and I can only say how grateful I am for the work you do and for presenting your findings in a language so that someone like me can understand. “Follow the money” to understand current day capitalism has been my mantra for a few decades now and it disturbs me to see the erosion of principles of respect for fellow humans.

Great post – as usual – and depressing to see usual suspects involved – Sir Rory with his 200 million plus from Merck and Server with connections to, and funding from, everyone including the new (to me) Foundation for circulatory Health.

What’s going on here seems exactly the same as the activities of research bodies in other industries designed to muddy the water – Sugar Bureau, tobacco foundations, oil company funded think tanks.

There’s a great film on the tobacco research in which charismatic PR guy explained: ‘our product is doubt’. Certainly doubt seems the most important ingredient in latest round of statin research.

We kind of expect companies to do this kind of stuff but when doctors are involved it seems much worse.

What puzzles me though is why all this frenetic activity for a drug that is off patent?

Is it that statins and cholesterol dangers are intimately connected and if cholesterol isn’t the demon then what happens to PCSK9 drugs?

Although that doesn’t fit with the main thrust of PCSK9 promotion which has been to stress that they are a solution to the ‘statin intolerance’ problem that apparently affects 25% or more of patients who need the drugs. Maybe the manufacturers should be the ones unravelling the nocebo paradox

Well, as an old researcher in the natural science of metallurgy I can easily understand that if your intention is to hide obvious results of you research this can easily be accomplished. However If your mind set is working along theses principles in your own “research” of medicine (although unbelievable in my own field of superalloys) you are just corrupt one.

And when you are at the same time sacrificing the health of your fellow citizens your are at the bottom of my scale of disgrace.

I am on my second statin type after muscle problems with the first. My doc has just halved the dose because of more adverse muscle reactions. My thigh muscles have shrunk over 3 inches, initially put down to 12 days hospitalized but now statins suspected. thigh pain seems caused by shrinkage of tendons as well. All stopped when I stopped taking statin but my cholesterol levels rose. Now very low cholesterol again but muscle pain back. There seems no wins in ageing

I used to be interested in the trigs/HDL ratio – mine went from nearly seven to around or usually less than 1. Having consistently achieved that – by eating the exact opposite of what I was told – I have become totally disinterested in my LDL.I also no longer bother with the tests.

Having spent over fifty years being alternately marinated in glucose, then insulin, no I don’t expect to live much longer, the last twelve years are unlikely to undo that much damage though I finally feel much healthier. And of course this will posthumously be blamed on eating too much fat and not enough starch, as were my ridiculous lipids and high BP etc. when in fact as with probably the majority of the population the cause was the exact opposite. Oh of course “statin deficiency” will also be in there as a cause. Sigh.

Ouch! patrickgoff, why would you want low cholesterol when statistics have shown more deaths in people with lower cholesterol? We all need cholesterol! I gave up believing that gumph after my muscles shrunk, my tendons pulled horribly tight and my brain stopped working.

Quit taking statins Patrick – you don’t need to lower your cholesterol after all. There are studies proving people with high cholesterol live longer without heart attacks than people with high cholesterol. People who go on ketogenic diets (high in HEALTHY fats) lose weight even. You need cholesterol for several metabolic functions including converting sunlight to vitamin D, creating hormones, and building brain matter.

After 3 years of statins I had developed T2D and had so much muscle damage that I could not put my jacket on without help. But there was something more insidious! A year after I stopped taking the statins . . . well into my recovery . . . my wife said I had stopped walking like an old man, I was no longer stoop, I was no longer had my previous sharpness (such that I had). I now call statins my old-men pills.

A word of warning. muscle damage is one thing . . . if the damage extends to nerves that is not so easy to recover from.

Agreed, Anthony Sanderson. I can testify to that. The tendons in my feet, though much better, are still tight and the neuropathy symptoms continue….four years after stopping. Not good. Still, at least now that I know that it’s all in my mind I feel much happier about it all.

JanB
I was disgusted when I found about statins/Ezetrol and tendonipathy. Don’t understand the mechanism, take it to be a lack of cholesterol rather than an insidious side effect. I too have had problems with tight muscles still after three years, and I work at it by stretching the areas as I note them

What boggles the mind about lowering cholesterol is the fact that you need it in every skin cell as sunlight converts cholesterol to Vitamin D! So I assume if you lower it to ridiculous levels (under 1.0, which I had for a time after my heart op on 80mg a day), it’s having all kinds negative effects on who knows what in my body. I think pain is just the tip of the iceberg.

I assumed that ‘putative AEs’ meant the AEs they were recording, but given the tone of the paper with a suggestion that the AEs might not be real. My question here is – if you don’t ask specific questions at the point of recording when will you ask, there cannot be a better time? The reality is that the original study was not ‘specifically’ about side-effects so there was not that interest in the detail.
My own interest is more the biochemistry/physiology & systems evolution than the medicine, though obviously I am interested in health, on which basis I find this bad cholesterol thing total nonsense, but not having any clinical experience I never know if there are subtler things I don’t grasp. But, Dear Dr M K, you are plugging that gap and it does seem to tie up.

I think so, perhaps, but since no-one appears able to write in English in this paper, it is difficult to know. One good tip I was once given was the following. ‘If you want to spot the lie, look for mangled syntax.’

Well, I know of people who had cognitive impairment while on statin, and it reduced significantly when they stopped taking it. Anecdotal? yes, but it must have been the placebo effect. Of course there are hundreds of people dying who are not on statins, probably thousands but more likely tens of millions of people a year. That is the problem of living, at some point most people are likely to die, but Peter Sever (there are some amusing puns come to mind with a name like that) has no business putting the word “because” in the sentence as it can’t be justified. To use your quoted circumstance of the parachutes, it would probably be true to say someone who jumped from a plane above 100 feet died because they did not wear a parachute. We could do a hundred such tests and discover all most all of them died. Not so with statins, there is a gnat’s **** of a chance it might prevent someone dying, but not in the long term, and not without the risk of debilitating effects. (“Side” was deliberately left out). I wonder if Peter Sever is a friend of Rory Collins.

I wonder if any of these “experts” are on statins for any length of time. If there’re not they should be force fed the stuff for a few years!
I recommend a low dose of 20mg twice a day, say for five years.

“Specific questions relating to any putative AEs were not asked at these visits.” I take this to mean, after looking up “putative”, that the researchers did not bring up or prompt any known or suspected side AE’s with the subjects.

From my experience with the conduct of clinical trials, when recording adverse events researchers are specifically instructed to be as casual as possible. To ask patients “How have you been?” and see what crops up.
Their answers are then recorded verbatim in the case report form. If a patient says “felt woolly headed” then that is what is recorded, word for word, in the case report form.
My understanding of the “putative” phrase in question is that they are making a point of stating that questions were not specific.
What happens then is the interesting bit. All these funny phrases have to be consolidated, interpreted, categorised etc. Then someone, somewhere, decides what stays as an adverse event and what becomes an adverse drug reaction.
Before I become too outraged at the conflict of interest I would like to know more about the data interpretation.

I agree with PeggySue’s analysis, although I think “putative” means “assumed to exist or to have existed”, which is a way of indicating that these aren’t “real” adverse events but ones that are marked down.

I have always used putative (rightly or wrongly) to to mean something like ‘reasonably possible’ or ‘generally/reasonably accepted as the case’. . . So you might say ‘he was the putative father’ . . . in other words ‘It is proposed he is the father’ . . . with a little hint of : “likely but this might not be the case’.

My guess is that ‘putative AE’s’ at taken as ‘reported events that will be treated as real AE’s ‘ . . . with a little hint of ‘even though they may not be’.

So when I read ‘putative AE’s first time . . . my internal translation was . . . ‘so-called AE’s’ said with a bit of a sneer.

Dr Kendrick, I really admire your tenacity. Thank goodness for you and people like you, who continue to work for truth and ultimately the health needs of the population at large, and to push back against financial conflicts of interest.

For ordinary people like me, we become disabled by the giant power machine of those who want to sell more drugs. Who wants to listen to our words of caution?

I can help a bit here as I used to work at a trials unit and I’ve just had a quick look at the ASCOT-LLA 2003 paper. The adverse events were written down verbatim (patients were seen at family practices in the Nordic countries). To make things consistent, and easier to analyse, the written text was then coded to reflect its content; it seems this was done by a separate study monitor (i.e. not the person completing the form with the patient). The data were then transferred to the central database. The coding system used was:https://www.meddra.org/how-to-use/basics/hierarchy
The flowchart gives a good example of how a report of ‘feeling queasy’ would be coded.

‘Putative’ in this context just means that no suggested adverse events were made to patients, so the study nurses won’t have explicitly asked “have you experienced any unexplained muscle pains in the last few months?”.

You are correct, but what isn’t said is that the MedDRA dictionary, though available in a dozen languages, it is not available in any Scandinavian languages. As these medical practices were in Scandinavian countries, it would seem that some translation would be required. How this was managed is not reported, but it seems as though it would give the trialists (in the employ of the drug companies, directly or indirectly) the flexibility of judgment that could enhance the likelihood that outcomes favorable to the drug companies would be reached.

Mr Chris…..until a few decades ago, pharmacists routinely removed inserts from medications.
We merely received prescriptions from the Dr with brief instructions telling us how and when to take tablets/liquid mixtures/creams/lotions.
It was a great leap forward when we were actually allowed to read the detailed instructions as per the manufacturer. I reckon that is when some bright spark thought that we were imagining the side effects! What a farce the whole situation has become.

When I queried my (ex) GP about the inserts and the info they contained he told me to ignore them, apparently because he thought it was rubbish? Or maybe not for the eyes (and brain) of the hapless patient.

He said it was a “tragedy” akin to the MMR scandal that high risk patients had been deterred from taking drugs which could save their lives. Urging patients not to “gamble” with the risk of heart attacks and strokes, he said “bad science” had misled the public, deterring many from taking life-saving medication”

The CDC knew for 14 years there was a link between autism and MMR, as publicised by William Thompson, the senior researcher involved in the study. The CDC tried to destroy the inconvenient data. Taking drugs, administered by practicioners who, for the most part, did not know the ingredients of the vaccines, which could threaten the quality of life (brain damage). Though I understand there are vaccines which do not now contain mercury, all contain aluminium hydroxide. We should not use aluminium saucepans because of the risk of brain damage, so why is it life threatening to avoid multiple vaccinatiions of triple or even quintuple vaccines all of which contain aluminium, injected under the skin (safety barrier number 1)?http://www.greenmedinfo.com/blog/herd-immunity-flawed-science-and-mass-vaccination-failures
Peter Sever is guilty of using “bad science” to mislead the public, causing many to take toxic and unnecessary medication when it comes to statins. (Sorry for the off-topic)

“Myth 4: Drinking out of aluminum cans or cooking in aluminum pots and pans can lead to Alzheimer’s disease.

Reality: During the 1960s and 1970s, aluminum emerged as a possible suspect in Alzheimer’s. This suspicion led to concern about exposure to aluminum through everyday sources such as pots and pans, beverage cans, antacids and antiperspirants. Since then, studies have failed to confirm any role for aluminum in causing Alzheimer’s. Experts today focus on other areas of research, and few believe that everyday sources of aluminum pose any threat.”

AH Notepad: You’re welcome. This is apparently run by an anonymous scientist, and it is one of the best. The thing is, anyone, whether scientist, physician, or parent, who has read the research and history of vaccines knows how dangerous they are, but the industry is so powerful that they will destroy anyone who questions, so most scientists and physicians who know keep their mouths shut. Moral courage is exceedingly rare. This is why Andy Wakefield is near the top of the list of those I admire. He has it. They haven’t and won’t destroy him. Interesting that two of the scientists (from Columbia University) who ran a phony replication study of the Wakefield, Walker-Smith, et al. study are now in a cat fight in federal court. They were once a pair to draw to. The female half of the sketch was the lead researcher in a study of Hg toxicity in a mouse model in 2004, and testified in Congress about her findings, but received so much push-back from an anonymous blogger which caused her such problems with the university administration that she stopped all Hg research. Perhaps the crappy science they subsequently produced will receive an airing in court. That would be sweet.

I can’t see aluminum cans being a problem but aluminum itself? It’s a potent neurotoxin, how could it not be problematic especially when it is injected and at doses that one would never receive via food or other manners and to infants no less. The blog here has shown, if nothing else, that experts and studies are less than reliable and should not be blindly accepted, especially when common sense says otherwise.

My point was, why if we are told to avoid everyday sources of aluminium, is it ok to inject a salt which can be demonstrated to affect the nervous system. I would question whether aluminium saucepans cause a problem, but if you happen to live in a place where fluoride is added to the water, it causes the aluminium to go into solution, with a figure quoted of up to 800ppm.

And you believe that myth, right? Hmmmm . . . . we know that deodorants (underarm types) contain a LOT of aluminum and are a prime suspect in alzheimers. Antacids are another big source of aluminum and I believe there is, most certainly, a connection between those two things and alzheimers. One nice thing about science is that we simply don’t have to believe what THEY believe at all. If THEY want to believe there’s no connection, fine, but for many people there’s a definite connection, whether it’s “scientific” or not. Personally, I prefer to believe people I’ve spoken with who actually go to the work of tracking down what might have caused this or that illness/disease. What a scientist thinks is sometimes so biased I’m just not interested in hearing their paid-for stories.

KidPsych. Ho,Hum!…now fancy that, I learn such a lot on this blog.
25 years ago I was working under very warm conditions as a hospital ward nurse. In desperation, at the height of the summer, I resorted to using an underarm antiperspirant and became really quite poorly within a few days, being unable to close my upperarm to my trunk without severe pain. It lasted for over 2 months after I stopped using the product, which I blamed as the suspected cause, but without knowing why.
I wrote to the company because I wondered if there had been a problem with the batch. I received a very nice letter back, suggesting that I was an isolated case, and must have had an allergic reaction to one of the ingredients, which they said was likely to be aluminium. And would I accept £25 for my bother.
How come the company suggested aluminium as the cause? Why not any other ingredient? Why did they isolate aluminium as the possible cause? What did they know that I didn’t know?
So, the experts think everyday use of aluminium does not pose any threat? Just like the statinators believe there is no problem associated with statins.
Pull the other one….we, the public, have been treated as victims of human experimental trials for far too long.

So, the experts think everyday use of aluminium does not pose any threat? Just like the statinators believe there is no problem associated with statins.
Pull the other one….we, the public, have been treated as victims of human experimental trials for far too long.

Jennifer, I don’t even think it’s as systematic as an experiment, using us as the guinea pigs. I think it’s the simple pursuit of profit, always a short-term goal and the skilled scientific workers divorced (alienated) from their work and its consequences, chained to the treadmill of debt, who do the math for them.

In another thread I posed an answer to MK’s, ‘Where to next with this blog?’ that he asked awhile back, that our health is bound up with the nature of our political economy; capitalism. The great majority of comments here, end up pointing a finger at big Pharma or Big Govt as the culprit, and the pursuit of profit at all costs, largely our cost and that of the environment.

It’s now abundantly clear that there is not a single aspect of our planet, down to the bottom of the very deepest ocean, to the space around our planet that has not been corrupted by the venal hand of capitalism. I mean, apparently even the humble drip dry shirt has been shedding microscopic particles that now occupy a permanent part of what used to be the biosphere, with the accent on bio.

Well anyway, my plea got not a whisper of a reply here and perhaps that tells me something about our complete lack of collective responsibility for what, we as citizens of the so-called developed economies, have done to the planet; ripped of the 85% and left them a garbage heap as payment.

I’ll try to find the info again, but apparently, the original study that found aluminum to be bad for the brain (Alzheimer’s study) was deeply flawed because a solution used in the samples was loaded with aluminum. All the screaming headlines were apparently based on that one original study. Just saying we all need to do some detective work before setting something in stone for all times.

I suppose that any clinical observation such as a new ache, only becomes an AE when has been accepted as being caused by the drug. Prior to that it is a “putative” AE since it may have an entirely unrelated causation?

An adverse event is something that occurs during the trial and is reported verbatim, regardless of causation.
If eventually they decide it is drug related it becomes an Adverse Drug Reaction and will go on to be listed in the side effect listings on pack inserts.
This is supposed to be done according to well established protocols but perhaps there will shortly be some newer ones available to suit circumstances.

Exactly. But most people simply get their news through the mainstream media and they’re happy to publish press releases. Sadly, Lancet’s publication gives some superficial credibility to the press release.

Putative in the context of this paper Malcolm, having given this some more thought, could be replaced by presumed, which opens up even more subjectivity over interpretation, which 15 years later then gets nicely cleaned up. This smacks of Keys all over again as his data collection was seriously flawed and his interpretations Putative!

“Specific questions relating to any putative AEs were not asked at these visits.” I’m thinking this means they were not asked about side-effects, the patients had to self-report?
Was this ASCOT trial data released, or is it considered “commercially sensitive”?

How much influence does the mind have over function of body? I suspect genes could be turned on/off under influence of what the mind perceives. Evolution might not be random but could be guided by thoughts/needs of the organism. Darwin’s finches come to mind.

Dr. Kendrick, thank you for continuing to spotlight the latest turn of the worm in the ongoing cholesterol con. I have a question that I hope will be of interest to you and your readers.

To recap: The current “nocebo’ study is a reanalysis of a much older study, ASCOT-LLA, which was a two stage hypertension trial with two groups of participants in each stage. It began with an initial blinded phase that was followed up by an unblinded phase. During the initial blinded phase, neither of the two groups of participants knew whether they were taking a statin drug or a placebo. During the followup unblinded phase of observation, both groups fully knew that they were either receiving, or not receiving, a statin.

The ‘nocebo’ effect proposes that people will manifest a higher rate of side-effects when they know that they are taking a drug that may cause side-effects. In keeping with this theory, one would then expect to see a considerable increase in muscle-related side-effects among the drug treatment group during the unblinded phase of the ASCOT-LLA study. But that is NOT what happened. Instead, reports of muscle-related problems DECREASED, from 2.03% to 1.26% (for an overall decline of 38%), within the drug treatment group when the study shifted from the blinded to the unblinded phase. At the unblinded phase, however, we do also see that the rate of muscle-related problems in the drug treatment group is somewhat higher relative to the non-treatment group (1.26% vs 1.00%) — a finding that the current authors now wish to attribute to the nocebo effect. But, if the presumed nocebo effect was really at work, why wasn’t there also a corresponding increase in the total rate of muscle related problems within the treatment group itself. Again, why was there an overall DECREASE of 38%? And what does this portend for the credibility of a ‘nocebo’ effect at any stage of the study?

You’ve already taught us to take medical headlines with a huge grain of salt and the work you’ve put out has been life changing for so many. Take good care of yourself and loved ones; we want you as healthy as you help to make us.

Few people are providing such comprehensive information on the myths surrounding heart disease, but there are several people and organisations who digging deep in the vaccine field. I think a case of horses for courses.

So difficult to try and have another view, another way. Only anecdotal for some of us, but anecdotes are powerful and meaningful for those of us with grandma’s remedies.
I am currently using turmeric paste and curcumin capsules for my dog with osteosarcoma.
She is comfortable, my lovely vet thinks I am a little deluded and I will certainly use what she has to offer if things go tits up.( sorry for profanities) .
Dr Kendrick, you are remarkable and you may need us as your Dad’s Army, so keep yourself fit folks, you may be called upon. Though my heart is breaking for my fur baby, you can count on me.

Perhaps all those that are so confident that statin adverse events are in the mind should start taking statins as a show of their confidence in them. And if the crippling muscle pain doesn’t get em maybe their memories will be impacted to the point that they forget their cause.

If these “nocebo” results are based on test subjects taking 10 mg of atorvastatin vs a placebo then I would suggest that this is not a fair trial of statins vs placebo as 10 mg is the smallest dosage size available. Duane Graveline discusses low statin dosage (5 mg) here: https://spacedoc.com/articles/a-case-for-low-dose-statins . From Dr. Graveline’s article and other more recent publications, it seems that the beneficial (pleiotropic effects) of statins occur with low dose statins.

Given the very low levels defined by the current “cholesterol guidelines” I doubt that many people are taking such a low dose (10 mg atorvastatin/Lipitor). Dr Graveline suggests that adverse side effects of statin treatments increase with increased dosage.

The low statin dose might have given these “researchers” a softer ball to play with.

Some 80% of patients are statin tolerant. In the HPS study of the 40,000+ that made it into the final selection which include taking a statin, 20,000+ were selected – ALL known statin tolerant. Of course the numbers excluded for statin intolerance were never divulged but the tolerance to statins in these known statin tolerant patients was used as a bench mark for statin tolerance

Some 80% of patients are statin tolerant. In the HPS study of the 40,000+ that made it into the final selection which include taking a statin, 20,000+ were selected – ALL known statin tolerant. Of course the numbers excluded for statin intolerance were never divulged but the tolerance to statins in these known statin tolerant patients was used as a bench mark for statin tolerance

Duh? Am I missing something here? If all the people in the study are statin tolerant then it stands to reason that they will NOT exhibit any of the symptoms that those of us who are statin intolerant suffer from. How can you exclude the very people that you are meant to be examining for ‘side effects’?

Why the heck are you taking any medication? Even assuming these numbers mean anything (a big IF), yours are well below any recommended level. Moreover, low TC is associated with higher death rates. TC below 150 is particularly bad, especially for cancer and accidents. I’ve always had low TC and have taken steps to increase it, not decrease it. The overall death rate for TC is a bathtub curve — high at low and high cholesterol levels. If you think lowering your cholesterol below 150 is somehow “good”, I’d reconsider.

Charles, consider yourself lucky to be on the good side of the bell curve. My understanding of statins is that cell function is altered. Probably every cell is affected in some way hence multitude of symptoms. Small dose over many years could lead to unexpected results. Focusing on cholesterol is a red herring.

Charles, you might want to read Dr K’s book “The Cholesterol Con”. Not the only very good book on that topic either. My own view is that even if someone taking statins does not have any noticeable adverse effects, there may be some harm going on that isn’t obvious or noticeable.

I’ve had to have my blood tested recently, and the GP is running tests for things that might be related to my symptoms/possible health problem. He also wanted to test my cholesterol and I said if he wanted to know what my cholesterol levels are that’s fine, but I will not be taking statins.

TC 146 mg/dl translates as 3.8 mmol/L . . .
I have been convinced that total cholesterol is not a good measure of assessing vascular health. . unless it is too low which indicates a increase in overall mortality . . . especially in older men (say over 60) . . . 3.8 seems rather too low.
HDL looks good
TGs even better
I’m not in danger of being struck off . . . so I can say: I do not know why you are on statins.

Charles, regarding your arterial plaque question, there is this presentation on youtube by Nobel Prize winning (twice) bio-chemist Dr. Linus Pauling, who, at 90+ years of age, said he assumed L-lysine at 7 g/day, combined with vitamin c at 3 g/day, has helped a colleague of him rather spectacularly. These are doses that sound ridiculously high, but considering the fact that orangutangs in the zoo (not the W.H.) are on a ‘budget’ of 10 g/d, to be given through fruits and vegetables also.
10 g/d vit c + 3 g/d L-lysine didn’t kill me after 2 months, the only side effect was a lowering of BP by 20 points (one measurement only) and a much higher ability to exercise before getting out of breath.
Of course this is all very anecdotal but I was so impressed by this presentation of him, and the way it made sense to me, that I decided to just try it out.https://www.youtube.com/watch?v=2bymKIPaTws#t=2791 is where he starts about the L-lysine.

Phil, your point seems a strong one to me. 10mg is a low dose, too low to shed light on statins as currently prescribed. In my case I took 40mgs of atorvastatins daily for 13 years with no apparent ill effects. My dosage was doubled two years ago. I have had muscle pains, tiredness and stiffness ever since, even though I have not touched statins for 20 months.

Surely, writing the report in Klingon is deliberate? Fully 99% of the people who read this report, will not have a clue as to what it’s actually telling them, and I’m one them. I’m not a statistician, or a mathematician so how the hell am I meant disentangle the meat from the fluff?
The only sure thing to emerge is the fact that pretty much everybody involved in creating the report seems to be in the pay of the pharmaceutical industry. Talk about being blinded by ‘science’.

Ha! I’m not even a star trek fan and even I was able to get your message about the Klingon language. You are so right and this is a very apt way to describe it. Mind if I use your phraseology? I think scientists spend more time figuring out how to disguise their findings than they do actually trying to be productive members of the medical society. What a cotton pickin’ shame.

This is only too true Stephen. I was looking at a metanalysis of studie of MMR and Thiomersal/mercury in vaccines published in Sydney in 2014.
(https://www.ncbi.nlm.nih.gov/pubmed/24814559)
The study was not powered to cover all vaccines, but the author overgeneralised in his conclusion and the article was headed “Vaccines are not associated with autism: an evidence-based meta-analysis of case-control and cohort studies.”

The error was repeated in the abstract and quoted by the head of the Australian Medical Association, and in the Sydney Morning Herald.

That error got past the author, the editor and the peer reviewers and everybody else.

Andrew: Of course, meta-analyses are only as good, or crappy, as the studies which they analyze. The Verstraeten study, as published, is a good example of the latter. The Vaccine Safety Datalink, which the CDC zealously guards from prying eyes, was the source of his data. The findings were alarming in the first run of the data: compared to unexposed children, for those receiving 25 mcg Hg in the first month of life the RR for neurological disorder (by age six) was 1.8, autism 7.6, sleep disorders 5.0, and speech disorders 2.1. This would not do, of course. The gripping story of how the public health authorities magically transformed thimerosal into something no more dangerous than a box of Wheaties, including the secret meeting at Simpsonwood, GA in June, 2000, is told in “Thimerosal: Let the Science Speak.” It is telling that the the study you link to was published in Australia, which is rapidly becoming a Pharma paradise. Beginning next summer Australian parents will have to pay a monthly fine if their children lack a single dose of what the all-knowing bureaucrats recommend.

I’ve been following the Tim Noakes trial and can’t believe they are going after him again in appeal. There’s a petition going around that I signed recently if you haven’t had a chance yet. My ‘respect’ for Dieticians will never recover after this; I follow the ‘rebels’ now 😉

Thus his assessment is now subjectively affected – so it is possible that his attention and reporting of adverse events in patients he knows to be treated are simply ignored.
How many of us have told “statins do not do that” Also BAYCOL was taken off the market for killing but as Dr Graveline pointed out deaths from rhabdomyolysis have not reduced after its removal.

The slightly raised risk
This is another gross underestimate but then underestimation of adverse events. Furthermore, as the Medical Establishment and the NHS are way out-of-date on the science of diabetes, I for one would not believe anything they promoted. After all their protocol for diagnosing diabetes is based on hyperglycaemia and HbA1c, while hyperinsulinaemia is a diagnosis for early diabetes when there is a good chance of full recovery (Ref: Kraft MD MS FCAP, Joseph R.. Diabetes Epidemic & You)..

It seems to me that the medical establishment’s target is simply to “manage”; which of course maintains Big Pharma profits which can be substantial.

If memory serves the ASCOT trial was first published in 2001 (J Hypertens 2001;6:1139–1147) Since then it has spawned a series of studies authored by Severs et al. I note too that the current paper is
Funding These analyses were supported by an unrestrictive grant from Pfizer
Commercial funding has always proved subject to limitation because of “confidential data”

In their report from the lipid-lowering arm of the ASCOT-LLA trial Sever et al concluded that statin treatment may have pleiotropic effects able to lower the risk of infection and respiratory illness even eight years after ending the trial.[1] They mention a few unimportant limitations, but have ignored the most important one, the fact that during these eight years 37% in the treatment group had stopped the statin medication whereas 56% in the control group had started . It is not too farfetched to assume that those who stopped the treatment did it because of unpleasant adverse effects, and that many of those, who had started it, not yet had recognized that possible adverse effects were caused by the treatment. Thus, the higher incidence of infections and other pulmonary diseases in the control group could as well have been an adverse effect of the statins .

That cholesterol-lowering should prevent infectious diseases is also unlikely, because the lipoproteins protect against all kinds of infectious diseases.[2,3] Furthermore, low cholesterol has been found associated with infectious diseases.[4] Most authors assume that the low cholesterol is secondary, but this is contradicted by Iribarren et al.[5] They followed more than 100,000 healthy individuals for fifteen years. At follow-up, those with the lowest cholesterol had been admitted significantly more often to hospital because of an infectious disease. Evidently low cholesterol, recorded at a time when these people were healthy, could not be caused by a disease, which they had not yet got. Another argument was presented by Sijbrand et al.[6] They found that before the year 1900, when infectious diseases were the commonest cause of death, people in the Netherlands with familial hypercholesterolemia lived longer than the average Dutchman .

“The benefits of statin treatment in both primary and secondary prevention of cardiovascular disease (CVD) have been well established…” I have noticed this phrase being used on many statin study as a preamble. My reaction is that the study is sponsored by a drug company that wants to promote their product and the researchers will do their utmost to comply, otherwise no more grant money.

Well as far as I know, everyone dies. There was a guy over 2000 years ago but that’s just an anecdote . . . what they actually mean is “lives extended”, but often not by much, and with the quality destroyed.

In the double-blinded phase of the trial, muscle symptoms occurred at the same rate—2.0% per year in both the statin and placebo groups.

I suggest that the attending physician would as he examined the lipid profile immediately be able to identify the treated from the placebo patient. If he couldn’t well…..

Thus his assessment is now subjectively affected – so it is possible that his attention and reporting of adverse events in patients he knows to be treated are simply ignored.
How many of us have told “statins do not do that” Also BAYCOL was taken off the market for killing but as Dr Graveline pointed out deaths from rhabdomyolysis have not reduced after its removal.

My old dentist, who carried out clinical trials, told me that in many cases the difference between patients was significantly greater than the difference between toothpastes – except in one case where the stuff was so much better the trial effectively unblinded itself.

I also recall a study – true or apocryphal I don’t remember – where priests were given LSD. The placebo group were saying things like

“I think I may be feeling something, I don’t know”

while the experimental group were weeping and saying “I see God!”

Yes obviously any patient whose LDL drops significantly is on the statin (unless in rare cases they become hyperthyroid).

They are making up their own rules for reporting as they go along. It’s like hermeneutics on demand. What you are doing is trying to figure out just what those rules were and what they mean. Or, perhaps closer, you are diagnosing a disease that only presents itself in a complex of seeming jibberish. But because the rule book here is meant to be hidden your recreating their obfuscation will be difficult at best. Please, press on.

Malcolm, Thanks for your efforts. Without even reading the paper, it’s simple to conclude it is junk science. First, it is surreptitiously industry-funded. Second, it is a distant post hoc analysis of an old and potentially unreliable database, done by authors with a vested interest in a certain outcome. The original study was not performed with side effects as primary endpoint. Third, the event rate is ridiculously low based on real world experience.
I wonder what John Iaonnidis would think?

‘Reports of AEs by the study participants were initially recorded verbatim and subsequently classified with use of the Medical Dictionary for Regulatory Activities into 26 separate system organ class (SOC) groups, 2288 unique preferred terms, and 5109 separated low-level terms…..’

Malcolm, you have a genius for homing in on the paragraph most likely to contain the crime! Sentences like that exude a sense that they have been worked on for ages to conceal something!

I have puzzled over how the crime was committed ever since I first heard of the idea tat people got the same number of AE’s on statins as on placebo. Because I was stupid enough to think Simvastatin was really good for me, and that ‘muscle pains’ meant something analogous to what you can get after walking a bit too far, I damn well know what happened to me wasn’t a nocebo effect.

My vague guess is that muscle pains are deemed low level, and are thus mixed up with a lot of other low level stuff like skin rashes, headaches, feeling off colour etc – thus diluting the damage the statin did – or maybe the placebo contained something noxious?.

It seems to me that there is an obvious way to score these results. Randomly pair people from the statin arm and the placebo arm, and ask an independent GP (you?) to try to pick out which person from each pair was on the statin! If you could do that with statistical significance, then the statin is causing AE’s! If statins have no AE’s, nobody – however anti-statin – should be able to pass that test.

Maybe. Of further interest is that if you ask people, not taking part in a clinical study, of any kind, about adverse events e.g. headache, muscle pain, in the last few weeks the rate is far higher than in any clinical study, either placebo or treatment arm. And these are people in their twenties. German study.

Pain, especially, is something one quickly forgets. A merciful Nature seems to have arranged things that way. So asking people about their pains at six-monthly intervals is guaranteed to substantially under-report any pain felt.

These days when everyone has a smart phone, patients in studies should be given an app that intermittently asks them to input any symptoms they are experiencing at that moment. It would have far stronger statistical validity than any questionnaire conducted at lengthy intervals.

Likewise my Simvastatin took 3 years to produce side effects. Maybe as the body ages, it can’t tolerate quite as much statin – who knows because they can’t do research on the problem without admitting it exists!

For me it took just over 3 years for simvastatin’s damage to manifest itself; however, my wife says that I had aged well before the pains etc appeared. Without the statins I have turned the clock back physically and intellectually. (Think the ‘other half’ might want to qualify the intellectual bit somewhat)

What about all those people who never question anything, take all the pills that are assigned to them, live their lives very afraid of getting a CVD or a stroke, and are even more afraid of getting scolded by the doctor, have a very, very low “blood cholesterol level” and still they end up suffering a heart attack or a stroke that makes the last years of their lives a living hell. These people have done everything *right*. They are very obedient patients. And there is no hope for them…

At some point, people should realize that the best public health policy is to do less, instead of more.

Medicine is an art. There is dignity in art. There is not dignity in destroying people’s lives for a greater good that don’t exist.

In the long, distant past, only rich people could afford to see a doctor, and suffer the consequences. Today, everyone has to go to see a doctor, there is no alternative. And everyone is at a high risk of being humiliated, manipulated and finally damaged, perhaps greatly damaged, by a well meaning bastard, by a very sophisticated brute. Doctors have to may more attention to what is right in front of them. Please, forget the great ideals of science. Forget social justice for a little bit. Just concentrate in the person right in front of you. If there is no real person in front of you, and you only have numbers and your feelings and your imagination, then you are not practicing medicine, but only playing politics. Humanize yourselves or leave us alone.

Dr Kendrick started the series of roman numerals with the notion that he could provide us with enough giudance and clues that we could figure out for ourselves the causes and mechanisms of heart disease and thereby understand how the problem might be addressed or, better, avoided in the first place. That is the best way to learn – provided important but distracting sidetracks don’t take over.

What we learned:
Endothelial cells get damaged by physical and/or emotional stress, smoking, etc. A blood clot forms over the damage. Precursor endothelial cells in the circulation form new endothelial cells to cover the clot. The red cell walls account for the cholesterol now within the vessel wall. Other blood cells (repurposed endothelial precursors) infiltrate the clot (plaque) from the vessel’s lumen to break down the clot and carry it off. Healing. It’s probably more complex than that, possibly involving the vasa vasorum, etc.
We know that vitamin C helps to keep healing ahead of accumulating damage, plaque, and calcification.
We know that increasing nitric oxide helps the endothelium do its job. L-arginine, potassium, etc increase nitric oxide.
What we don’t have is a detailed and exhaustive list of actions to take, actions to avoid, substances to favor ingesting and avoiding, and the assurance that we understand all we can about the whole process.
All those etc’s!

I think the idea that we (I!) can figure it all out is a tad optimistic.
So, notwithstanding my acceptance of the importance of this particular blog entry to the wellbeing of the naive public, I was disappointed that this was not the next roman numeral with further clues and guidance.
So much to do. So little time.

JD Patten
I think you are a tad optimistic if you thought this series was going to be “instruction Manual for bodies” . I think we have received enough information to make our own minds up, we are all different, the principles are there, make up your own manual.
What I note is that each contributor has his own solution to his problems, which work for him. I note that in spite of being told that diet is only A factor, a lot of the comments are about diet. I note the that in spite of it being suggested, that unless the cholesterol figures are way out of whack, you should not get fixated on them, that nevertheless there are a certain number of posts that have not assimilated this fact.
I have always thought that I have one body, one health capital and it is up to me to work out a lifestyle that keeps me alive to read this excellent blog

Mr Chris,
Your “notes” are right on point. Well taken.
However, no one is entirely self sufficient in this complicated world. Your manual is surely constructed from bits and pieces from others that you’ve examined – to the degree that any one individual can, I presume – and incorporates what seems to fit you. Only your own life can tell you whether you chose wisely for yourself. (End points! 🙂 )
The best research using double blind randomized controlled trials is only good to see what applies to Mr Average trial subject. Whereas, each of us is distinctly individual.
I still look for guidance from those with wisdom achieved from greater experience in their dedicated field.
My dedicated field is antique house restoration.
You?

Good news! Statins increase nitric oxide production! (Yes, I’m being facetious.) My apologies to linking to the dailymail, but I found the article fascinating.

Researchers propose here that it is not only cholesterol lowering that reduces heart disease, but also increased nitric oxide production and a reduction in the size of the heart. They appear to be working hard to find alternative reasons why statins supposedly protect against heart disease (outside of their intended effect). As Dr. Kendrick has noted, there are less invasive ways to increase nitric oxide production (including a little sunbathing).

‘By using the power of the large-scale imaging studies from the UK Biobank, this study indicates that statins may have a direct effect on the heart’s structure that we haven’t been able to detect until now. But we need more research to confirm this finding and understand the mechanisms involved.’

MK
Here is what I found on their site,
UK Biobank’s Principal Investigator and Chief Executive is Rory Collins, who is also British Heart Foundation (BHF) Professor of Medicine and Epidemiology at the University of Oxford.
Nuff said?

What the promoters of these drugs obviously hope will escape notice is that whether or not heart disease is the number one killer, all those hundreds, thousands, millions of people we are to believe will be saved from heart attacks by the drugs ARE ULTIMATELY GOING TO DIE OF SOMETHING, and most likely something less pleasant than a quick heart attack.

I, for one, would like your opinion on the work of Dr JR Kraft on insulin testing. For what its worth, his research on hyperinsulinaemia is highly relevant to the current obesity and diabetic epidemics, while the medical establishment is well and truly stuck in the Ancel Keys era of flawed hicarb research. However I admit that in recent years, the problem of sucrose has been “rediscovered” but with little recognition of Yudkin’s work back in the ’60s and ’70s. The medical establishment was wrong then as they are in 2017.

One wonders why. Are they so trained and brainwashed by Big Pharma (BP) that they only see “cure” as a function of BP’s chemicals and vaccines?

I realize it may not translate in this setting, but I have my law students and legal interns do grunt work all the time. I would be happy to be your grunt and assist you with anything that might help alleviate some of the burdensome or administrative things that don’t need your critical eye.

It strikes me now that to be able to perform sophisticated criminal activities, which I consider this type of “medical research” is a typical example of, you must, as any criminal, develop an internal psychological rational to be able to defend what you are involved in. I mean that no person can possibly stand the feeling of being “rotten” all the time.

I just wonder how this rational may look like for these guys.

It couldn’t possibly be “I get away with it since I am a smart guy!” – Could it?

Both drugs are similar in terms of %age of reports citing these two adverse reactions.

Following from this the Summary of Product Characteristics (SPC) of these two statins can be downloaded from the MHRA web site. The SPC of a drug is the nearest thing to a data release that is in the public domain. It is accepted as “true” by both the MHRA and the drug company.

Musculoskeletal and connective tissue disorders
Common: myalgia, arthralgia, pain in extremity, muscle spasms, joint swelling, back pain.
Uncommon: neck pain, muscle fatigue.
Rare: myopathy, myositis, rhabdomyolysis, tendonopathy, sometimes complicated by rupture.
Not known: immune mediated necrotizing myopathy. Wrong: This does occur! a David on Stop_our_statins has published photos of his devastated calves – he also sent the photos to Collins – never got a reply.

Alzheimer’s (AD)
Dement Geriatr Cogn Disord 2009;28:75–80 Midlife Serum Cholesterol and Increased Risk of Alzheimer’s and Vascular Dementia Three Decades Later: Alina Solomon et al
This study is one of the few looking at long term cholesterol and AD and providing hard numbers. Points to be noted:
1) patient records were trawled back over 2-3 decades to find high TC. Data on TC after finding high TC therefore must have been lower.
2) There are no patient records available on therapy. As this was data from a medical insurance company it is obvious that this data was simply hidden
3) Patients in the US are terrified of high TC and most would demand cholesterol lowering drugs (probably statins from 1987-1990).
4) It is likely that all patients with TC levels > 200mg/dl (circa 5.0 mmol/L) would have been treated
It is reasonable to assume that the lower TC levels found in the original high TC patients were a result of statin therapy post 1990
Odds Ratio Confidence Interval Calculation For 2×2 Contingency Table
Solomon A. et al report

Clear evidence that statins were associated with AD despite the deliberate hiding of therapeutic data. Incidentally 1.6% increase of AD is equivalent to the 1.5% of lives saved by statins over five years in the HPS study

MK/Moderator: PRIVATE MESSAGE TO YOU. PLEASE DON’T POST. I ain’t no lawyer, but I would consider whether you might want to take out the thing about how he “forgot” about his conflict of interest. I’d guess that here in the US, that could be libelous, since (at least according to the Lancet guidelines I posted), he’s entirely within the rules and has no obligation to disclose the more historic conflicts.

Yes, of course common sense says that those historic connections are quite relevant in trying to gauge whether there may have been bias here by the author, but I’d hate to see your excellent work distracted by being at the receiving end of a lawsuit, so you might want to word this some other way.

It strikes me now that to be able to perform sophisticated criminal activities, which I consider this type of “medical research” is a typical example of, you must, as any criminal, develop an internal psychological rational to be able to defend what you are involved in.

As much as I want to see the Collins, Severs et al as the statin bogey men of this world, I just can’t bring myself to believe that they truly don’t believe in what they are doing / preaching. It just seems unbelievable that well educated doctors would deliberately put millions of people on poisons which they know will ultimately harm them. Surely they must be driven by a (however misguided or erroneous) genuine desire to do good or am I just being naive? Surely they must genuinely believe that their clinical judgement isn’t being compromised or conflicted by their paymasters? Again, am I just being naive?

Mark Johnson: No, I don’t think you’re being naive. I think it likely they do believe that lowering serum cholesterol is the way to reduce CVD, and evidence to the contrary wouldn’t shake this belief even if presented to them. Churches are full of people like this.

Gary O: Confidence in medical profession would drop to zero in the eyes of the average consumer of pills if they are told that “bad cholesterol” does not cause heart disease and they can stop taking statins.

Andy S: There is truth in what you say; however, it is physicians like Dr. Kendrick, my own GP, and many others here in the U.S., who have actually raised my confidence in and respect for the medical profession. What they have in common is that first, they listen to the patient. The patient, like the parent for the children, has to be in charge of health decisions. The statin pushers, like the vaccine pushers, politicians, and media are stuck in a failed paradigm, and are incapable of, or too frightened to, fight their way out of it. I learned enough about statins before it became an issue in the doctor’s office that I was able to refuse them in advance of her suggesting them, and she has never mentioned them again. She can see my excellent state of health, and approves of it. But you’re right; this is why it’s all hands on deck for both the statin pushers and vaccine pushers. Public confidence is critical for their sales pitch, and this is in decline.

Gary O: You are fortunate to have an understanding GP. My experience with two cardiologists has been negative, pushing statins and condemning saturated fat. Thankful that Dr. Kendrick has invested time and effort to challenge faulty medical advice. The internet is the battleground in this struggle. Sometimes I wonder where I would be health wise without access to the internet, having to rely solely on medical advice from a GP.

The internet is the battleground in this struggle. Sometimes I wonder where I would be health wise without access to the internet, having to rely solely on medical advice from a GP.

Quite a few years ago now, not long after I had returned to the UK after living in Africa for around ten years, I signed up with the local surgery and had a ‘discussion’ with my then GP about my Thyroid treatment (or lack of) and the issue of searching the Internet came up. The guy flipped his lid as they say. ‘Oh another idiot relying on whatever crap you find on the Web’.)

I of course I told him that were the internet not around, I would resort to using my local library and pointed out that books can lie and mislead just as readily as a Web page, but that’s where I would be otherwise if I needed to know something (Karl Marx spent most of his time in London in the British library and some of his writing had over 150 separate sources, somebody even wrote a book about the vast range sources he used!).

The next time I saw him, he actually apologised to me. The thing is, for so long doctors have been regarded as something akin to a priest (and we know what they get up to), their word is sacrosanct. The Web blew that all away.

Actually, I regarded his initial response a deeply offensive and I told him so but he is implying (without knowing any thing about me except my underactive thyroid) that I too stupid to make analysis and come to a rational decision, which is perhaps why he finally apologised to.

I agree. I sometimes think that scientists get so used to twisting their minds round ‘impossible’ ideas – like Relativity, quantum mechanics, etc – that they don’t notice when they step over the line into falsehood.

Of course, the money and prestige also helps them to be confident they are right!

Edited post should read
From the article “At each study visit all adverse events (AEs) reported by participants were recorded by the study team in the case report form. Specific questions relating to any putative AEs were not asked at these visits.”

If they did not ask about specific side effects then their reported rate is a gross understatement. If you just ask people to tell you what side effects they are experiencing then you MISS most of them. This is a known fact in clinical medicine.

I had a CT coronary angiogram last week (long story, to do with my aortic valve replacement which may need replacing after only three years, it was replaced originally due to having been born with bicuspid aortic valve), and I got the results yesterday: calcium score 0, all coronary arteries clear. I have high cholesterol, have had high cholesterol for the past ten years, high as in the 8’s and 9’s total, but high because my HDL is high, around 3.5 – 3.8, and my trigs very low at 0.5.

I’m in my mid 60’s now. I’m on a high fat, low carb ‘Paleo’ way of eating: fatty meat – beef, pork, lamb, chicken with the skin, oily fish, green veggies always cooked in coconut oil (I need the calories the fat gives me), almonds, eggs, sometimes the odd bit of cheese and a nice glass of red wine with dinner (neither cheese nor wine are really paleo I know), no grain foods, no legumes or pulses, no sugars, no fruit, no starchy carbs (eg potatoes), no processed foods. I walk five or so miles a day, plus do a bit of weight lifting. Supplements: vitamin D3 and vitamin K2 (I have osteoporosis).

This time, since it’s been ten years I’ve been eating this way and since I have high cholesterol which, incidentally rose as I ate this way, it used to be so called ‘normal’, which worries my docs loads, yet I have completely clear arteries, I am going to let my cardiologist and GP into my little secret !
Anne

Can anyone help please? My husband had a TIA in 2010 and was put on statins and aspirin. He was in a very stressful job and had another in 2011. His statins were doubled but he started with leg muscle problems and after a few months, and reading The Great Cholesterol Con he stopped the statins against doctors advice. He was put onto clopidogrel, retired and has been fine ever since except that we have noticed he trips and falls a lot. We just put this down to clumsiness or perhaps the remnants of the statin effects – his legs still tingle and are occasionally painful. However, I came across something that suggested gait problems could be to do with the clopidogrel he’s taking. Does anyone have experience of this? I am wondering whether it would be a good idea to swap back to aspirin or stop it altogether? There’s no point in going to our GP as he already thinks we’re nut jobs.

Has this very recent study been mentioned here?
“Effect of Statin Treatment vs Usual Care on Primary Cardiovascular Prevention Among Older Adults”.http://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2628971
“Question Are statins beneficial when used for primary cardiovascular prevention in older adults?”
“Conclusions and Relevance No benefit was found when pravastatin was given for primary prevention to older adults with moderate hyperlipidemia and hypertension, and a nonsignificant direction toward increased all-cause mortality with pravastatin was observed among adults 75 years and older.”

I’ve just cited a paper about the effects of statins on older people. Here is another paper than appears to be relevant, although not specifically about statins. I don’t know if it has already been mentioned here:
“Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review”.http://bmjopen.bmj.com/content/6/6/e010401
“High LDL-C is inversely associated with mortality in most people over 60 years. This finding is inconsistent with the cholesterol hypothesis (ie, that cholesterol, particularly LDL-C, is inherently atherogenic). Since elderly people with high LDL-C live as long or longer than those with low LDL-C, our analysis provides reason to question the validity of the cholesterol hypothesis. Moreover, our study provides the rationale for a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly as a component of cardiovascular disease prevention strategies.”

Statins did not cause a meaningful reduction in heart attacks, coronary heart disease deaths or deaths from any cause in people age 65 and older, a new analysis finds.
`
The benefits of statins for people older than 75 remain unclear, a new analysis finds. Statins did not reduce heart attacks or coronary heart disease deaths, nor did they reduce deaths from any cause, compared with people not taking statins, researchers report online May 22 in JAMA Internal Medicine.http://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2628971

The ‘nocebo’ thing troubles me. There are thousands of medicines and many of them are accompanied by very long possible side effects – some of them quite extreme and even life-threatening. I bought over the counter thread worm tablets for my son recently and was shocked by the long list of possible side effects from a simple worming medication. So, if nocebo were a recognised thing across the population, wouldn’t we all be reporting far more side effects from the medicines that we take?

The vast, vast, majority of drug related adverse events are never reported, or recorded anywhere. How many here would report a headache after taking a medicine? Even if it happened within half an hour, every time you did so.

Which is as I suspected. So why are the takers of statins being identified as ‘noceboers’ and more likely to report side effects than takers of thread worm tablets? I must be missing some logical argument here by those who have decided about the nocebo effect with regard to statins – or are they just making this stuff up? (Which would of course come as no surprise!)

We have been “trained to obey” doctors. Never to question their superior knowledge and ability. There are a couple of doctors I respect this way, but their respect had to be earned. Sadly, there are many more I question on a daily basis, and their arrogance seems to know no bounds.

Very true. I finally connected my headaches with the nasal remedy, Flonase after several months of daily headaches. I asked the pharmacist about the possibility and he said that was likely. My doctor pooh-poohed it but did agree to a different medicine.

How do we ever change things, when doctors who are supposed to be representing our interests, constantly deny, smirk, and ridicule our protestations regarding these “wonder drugs”? We are imagining all that is happening to us, or so we are made to feel. Personally, I felt I was being ungrateful for what they were trying to do for me. Will it never end? 😥

Joyce, I’m happy to listen to my doctor but I decide. I never get the type of friction that others describe. If I did, I’d ask the doctor if he or she understood informed consent. It’s the law, as confirmed by the Supreme Court. How often is this respected on, say, statins?

Stephen, I agree with you up to a point. If I am well informed on a subject, (and forearmed) I am known by my G.P. for “sticking to my guns”. However, not everyone always feels well enough informed to argue their point. After all this is “The Doctor” you are questioning. (Shock, horror). Although I must have finally got through to him, as he was quite adamant that “he doesn’t take statins”, when I asked him! lol

And conversely when you significantly and majorly improve your health, but do so by doing the exact opposite of what you were told to do, as many many patients do, particularly in respect of diet, then you get told it is impossible and you must have made up your symptoms in the first place

There’s a way to go yet. Since you were “obviously” failing to comply with the diet when your tests got worse, then since you are “obviously” a known liar. when your tests get better and you claim this is from doing the opposite, you are still lying and actually “secretly” complying with the diet.

It’s taken significantly over a decade and undoubtedly many other similar tales from other patients for my GP to decide that perhaps there actually is something going on that she should know about.

Some of the others, not so much. They still warn patients about “cranks on the internet”, the “extreme dangers” of tightly controlling diabetes, etc. etc.

How do we ever change things, when doctors who are supposed to be representing our interests, constantly deny, smirk, and ridicule our protestations regarding these “wonder drugs”? We are imagining all that is happening to us, or so we are made to feel. Personally, I felt I was being ungrateful for what they were trying to do for me. Will it never end?

But can you imagine being a typical doctor with QOF targets to meet and a protocol to follow. In comes patient and the 10 minute countdown begins. Your last blood test results are in and QOF protocol dictates you need a statin. What’s the doctor supposed to do? And even if the doc stops believing in the pharmaceutical industry funded protocols, does he give up the day job? And isn’t prescribing drugs what the doctor has actually been trained to do? The doctor sets himself up for potential prosecution by not prescribing. Faced with that reality, what would you do?

Mark J: Things will not change, we have to change our perception of what to expect from the medical system. Consider doctoring as a trade. The service provided is a diagnosis followed by a prescription for a pill or an appointment with a specialist. The practitioner’s toolbox contains pills. The patient has to find his or her own way to maintain heath and avoid being prescribed pills. Where does medical industry rank as a cause of patient disability or death? The cardiologist has only statins in his toolbox for treating CVD.

Mark, I agree with much of what you say, but their escape from this difficulty is informed consent. If a doctor really doesn’t want to prescribe statins, they only have to discuss the pros and cons, as the law demands. If this were properly done, hardly anyone would taken a statin.

My previous entry on the Supreme Court’s decision on consent might be of interest.

Mark, I agree with much of what you say, but their escape from this difficulty is informed consent. If a doctor really doesn’t want to prescribe statins, they only have to discuss the pros and cons, as the law demands. If this were properly done, hardly anyone would taken a statin.

So does (or can) the enlightened doctor quote the figures for adverse affects he knows to be true, ie everyone will suffer mitochondrial dysfunction, CoQ10 depletion and in at least 20% this will transfer into aches and pains which in some will be permanent and possibly disabling and may even develop into rhabdo, serious heart failure, diabetes, cancer, memory loss etc. Or is the doctor obliged to quote the official line which will now no doubt state that statins have almost no side effects and it’s all down to the nocebo effect – symptoms that are “all in the mind”.

You state that: if this were properly done, hardly anyone would taken a statin.
How can the doctor now, “do this properly” without potentially getting into serious trouble?

When marketing rules
With ASCOT, the results were presented as miraculously positive. Like children, all the cholesterol experts instantly forgot past disappointments, notably ALLHAT. The only thing that
mattered was the present!
Including 20,000 patients, ASCOT was a multipurpose trial testing several hypotheses (like ALLHAT) and patients were randomised several times: first to groups who would, or
wouldn’t, receive an antihypertensive drug, then to groups treated by either a cholesterol-lowering drug or a placebo. In other words there were four groups of patients, but the authors
acted as if there had only been two: statins vs. placebo……..
Given that neither overall mortality, nor cardiac mortality, were significantly reduced, the discontinuation of ASCOT was not justified. In such conditions, and given the omnipresence
of the sponsor and the conflicts of interest, this trial remains quite dubious. In front of the totally negative results of ALLHAT, any objective observer could only conclude that the European Society of Cardiology was rather rash when it recommended the treatment of all hypertensive patients, independently of their cholesterol levels.
ANd

ASCOT and ALLHAT: when scientists disgraced themselves
……
Published in 2002, ALLHAT (Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial) presented the unique characteristic of being sponsored not by a company
but by independent public institutions. Despite a 17 per cent reduction in cholesterol levels, no protective effect was observed. As the trial included over 10,000 subjects, one could
hardly attribute this failure to an insufficient study population. This was very bad news for the statin industry.
I was attending a scientific meeting focused on cholesterol-lowering drugs in London when the ALLHAT results were revealed. All conversations around me immediately tuned to: “Are
the sponsors going to let us down?” “Will our funds run out?” “How are we going to subsidise our laboratories?” “How am I going to set up my next meeting?” “Where will I find new
grants for my students?” Scientific questions were relegated backstage and, during the three days of this meeting, I found no one attempting a reflective analysis of ALLHAT. All I heard
were moans and groans.
Then came a miracle!
About one year later, an article published by the Lancet reported on another trial testing the impact of atorvastatin in hypertensive patients. This was the ASCOT-LLA trial (Anglo-
Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm) of which Pfizer was the omnipresent sponsor.
The statistician in charge of quality control concerning the dataset and calculations was a Pfizer employee. Need I repeat that, since the implementation of the New Clinical Trial
Regulations in 2006–2007, this would not officially be possible?

Umberto
Dr, M. de Lorgeril has demolished the pro-statinist arguments in this book and in some of his research reports but the statinists simply ignore every point he makes.
Like all astroturfing agnotologists ie:Agnotology—the study of ignorance—provides a new theoretical perspective to broaden traditional questions about “how we know” to ask: Why don’t we know what we don’t know? The essays assembled in Agnotology show that ignorance is often more than just an absence of knowledge; it can also be the outcome of cultural and political struggles. Ignorance has a history and a political geography, but there are also things people don’t want you to know (“Doubt is our product” is the tobacco industry slogan)http://www.sup.org/books/title/?id=11232
In short The art of lying and getting away with it

So . . . I searched for “Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial 2002” to check what ALLHAT had to say on the lipid lowering treatment results. I found the paper (JAMA). There was no mention of the Lipid Lowering in the abstract . . . puzzle. Eventually I found mentioned in the conclusion that the ‘lipid lowering sub-trial’ was not dealt with in the paper . . . They implied that that part of the trial had a lot of participants and a 4-8yr follow up.

So I looked for the lipid-lowering sub-trial results . . . but in vain. The results that Prof. de Lorgeril talks about in his book seem to have been swept under someone’s carpet??

What I did find was a small piece about the ALLHAT results in the NIH’s “ALLHAT: Quick Reference for Health Care Providers – NHLBI – NIH”

To quote:
“The ALLHAT lipid lowering treatment study was conducted in a subset of ALLHAT participants; 10,355 individuals with mildly elevated LDL cholesterol levels were randomly assigned to receive “usual care” or drug therapy using a statin (pravastatin, 40 mg/day). Although the results of this nonblinded study are inconclusive, (whoa there . . . inconclusive!) they are nevertheless consistent with earlier trials (so they were inconclusive too???)and current guidelines to reduce blood cholesterol levels and decrease the risk of cardiovascular events through lifestyle changes and drug treatment“. . . . There then follows a couple more paragraphs of obfuscation.

Objectives
To examine statin treatment among adults aged 65 to 74 years and 75 years and older when used for primary prevention in the Lipid-Lowering Trial (LLT’) component of the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT-LLT).

Design, Setting, and Participants
Post hoc secondary data analyses were conducted of participants 65 years and older without evidence of atherosclerotic cardiovascular disease; 2867 ambulatory adults with hypertension and without baseline atherosclerotic cardiovascular disease were included. The ALLHAT-LLT was conducted from February 1994 to March 2002 at 513 clinical sites.

Conclusions and Relevance
No benefit was found when pravastatin was given for primary prevention to older adults with moderate hyperlipidemia and hypertension, and a non-significant direction toward increased all-cause mortality with pravastatin was observed among adults 75 years and older.

Antony,
Pravastatin happens the statin least likely to lead to type II diabetes.
I looked into it after I quit atorvastatin. Asked my cardio if he thought prava was good for a try. He informed me that his group no longer prescribes it. Weak. Not effective.
Don’t get me wrong, at this point no one will be able to talk me into another statin for myself. But, looking at this 13 year old study with some neutral perspective, you might admit that it’s no surprise the weakest statin should produce no effect.
Just sayin’.

There is no such thing as a weak or strong statin, it all depends on the dose. Pravastatin was used in WOSCOPS and many other studies and worked just fine – when the study was funded by a pharmaceutical company. ALLHAT-LLA was the only non pharma sponsored statin study – and it was the only one that did not show any benefit. An amazing coincidence.

Statins are statins, their adverse effects are directly related to their impact on human physiological system. Use pravastatin at a dose equivalent (in LDL lowering) to any other statin and you will find (I am certain) that it has all of the same adverse effects.

Can’t remember the name of the study now (or who sponsored it which is probably relevant) but I thought there was some difference between water-soluble or lipid-soluble statins, for example the former could cross the blood-brain barrier. Anyone with a better memory, or more enthusiasm for digging through the manure?

Possibly. Simvastatin, in theory, crosses the blood brain barrier more than Atorva – or maybe it is the other way round. I don’t know if anyone has really demonstrated any different impact on the brain.

Chris raised the idea that lipophilic statins and hydrophilic statins do seem to behave differently. I have read – (not in the above review) – that the lipophilic nature allows easier penetration in a cell (in principle) – so they speculated that those lipophilic statins were more effective in entering muscle cells, beta cells, adipocytes through the cell walls and were thus more able to do damage; hydrophilic statins causing less damage. (Not utterly convinced)

In the review above they deal with studies that show that there is an association between statins and diabetes. They point out studies that show pravastatin, when compared to others, is less likely to produce diabetes and raises the level of adiponectin (presumably bringing down insulin resistance) . . .. They raise the question of the hydrophilic nature of pravastatin . . . but then counter by saying that rosuvastatin (also in the hydrophilic category) – JUPITER study – is associated with increased chance of new onset diabetes.

Having said all this, the original point I was making, half a dozen comments ago, was that: Here we have a statin, albeit pravastatin, that lowered cholesterol – as required by the cholesterol/CVD hypothesis – but that it did not reduce CVD and if anything increased overall mortality (albeit not to an accepted statistical significance).

The important issue to me is not whether this statin or that statin is more or less damaging with respect to adverse reactions, but that the premise that cholesterol levels are the prime ’cause’ of atherosclerosis is wrong. So, taking a statin, any statin, for this reason alone is not a good idea.

Postdoc Tanja Kongerslev Thorning, PhD, from the Department of Nutrition, Exercise and Sports at the University of Copenhagen, is first author of the report. Tanja explains that scientists have long wondered why the actual effects of a food are at variance with the effects expected on the basis of its nutrition content. They have therefore started to look at things in a wider context:

“Researchers have become more skilful over the years, and we have acquired more methods for exploring what specific nutrients mean for digestion and health,” Tanja continues “But when we eat, we do not consume individual nutrients. We eat the whole food. Either alone or together with other foods in a meal. It therefore seems obvious that we should assess food products in context.”

Ultimately this means that the composition of a food can alter the properties of the nutrients contained within it, in ways that cannot be predicted on the basis of an analysis of the individual nutrients. For example, dairy products such as cheese have a lesser effect on blood cholesterol than would be predicted on the basis of their content of saturated fat. There are interactions between the nutrients in a food that are significant for its overall effect on health.

Tanja Kongerslev Thorning explains further “Another example is almonds, which contain a lot of fat, but which release less fat than expected during digestion. Even when chewed really well. The effects on health of a food item are probably a combination of the relationship between its nutrients, and also of the methods used in its preparation or production. This means that some foods may be better for us, or less healthy, than is currently believed.”

Some of the precepts of current nutrition science need to be reconsidered

The expert panel behind these conclusions consists of 18 experts in epidemiology, food, nutrition and medical science. They were brought together for a workshop organized by the University of Copenhagen in collaboration with the University of Reading in September 2016. Discussions focussed on dairy products, and on how the complex mixture of nutrients and bioactive substances, such as minerals and vitamins, can affect digestion and ultimately change the overall nutritional and health properties of a particular food.

The panel concluded, among other things, that yoghurt and cheese have a different and more beneficial effect on bone health, body weight, the risk of developing cardiovascular diseases, than would be expected on the basis of their saturated fat and calcium content.

Head of Department of Nutrition, Exercise and Sports at the University of Copenhagen, professor Arne Astrup, who chaired the workshop, explains that the example of cheese is good to illustrate that a food’s health effects cannot be judged by single nutrients e.g. sodium and saturated fat:

“In contrast to current recommendations that essentially ban full-fat cheese, current research clearly demonstrate important health benefits of cheese for prevention of type 2 diabetes, cardiovascular disease and cancers. All the positive effects are due to a complex interaction between beneficial bacteria, minerals and bio-active cheese ingredients.”

Professor of Food Chain Nutrition Ian Givens at the University of Reading, co-chair of the meeting, concludes:

“More studies are needed, but ultimately it seems that some areas of nutrition science need to be rethought. We cannot focus on a nutrient without looking at how it is consumed and what else is eaten at the same time.”

The findings are published in the article Whole dairy matrix or single nutrients in assessment of health effects: current evidence and knowledge gaps in the American Journal of Clinical Nutrition.

Story Source:

Materials provided by Faculty of Science – University of Copenhagen. Note: Content may be edited for style and length.

Errett
Another very interesting contribution but unfortunately behind a paywall.
This goes back to a general absence of proper nutritional studies in the human. In animals it is possible to put the individual animal in a metabolism cage and measure everything from heat loss, nutritional intake and feacal and urine energy loss. Indeed, it is even possible to measure the ruminal breakdown of food to absorbable “nutrients”
I have requested a reprint

Erret: Yes, we mustn’t forget the beef, although goat is my favorite ruminant (the fat tastes like high-quality butter). Hard to get, though. I just received delivery of a side of beef, 274 lbs., including extra feet, at my request. I also eat plenty of rabbit food, too, which I think is a good idea, if it is grown in healthy soil. The decline in the health of our soils, I’m certain, bears part of the responsibility for the decline in our health. Interestingly, I’ve recently given up fluid milk because of mucous production. Problem solved, and I’ve replaced it with-more cheese! On topic: My TG/HDL ratio has remained consistently about 0.5.

Sasha: Yes, the only milk I’ve had for about 15 years is raw, from cows on pasture, with the additional benefit of fermenting; high-quality stuff. I think I’ve just reached the point where I’m better without fluid milk (or at least fluid milk every day). But I eat lots of butter, cream, and cheese, so dairy foods don’t seem to have any negative effect, only positive. The butter, cream, and cheese from those same cows don’t produce excess mucous. Another dietary experiment. My mid-day snack is now usually nuts and cheese, rather than kefir.

One of my all time favourites is Vacherin Mont d’Or, like Brie with a turbocharger, but seasonal and off the market now until autumn/winter. Currently I eat various local varieties and some from further afield, including Halloumi which I cut into chunks and add to a Bolognese-type sauce and eat with runner beans, purple sprouting broccoli or asparagus (according to season) substituting for the pasta.

There’s a very creamy goat cheese which I spread thickly on an oatcake and stud with blueberries for a low carb cheesecake substitute. Deelish!

I’m also fond of goat meat but a word of warning – what I’ve had in the past was presumably kid, like lamb only more succulent and flavoursome. What I bought recently was a disappointment – obviously mature, more like mutton and needed a LOT more cooking than I gave it. Next time I’ll casserole it with assorted veggies and hopefully persuade it to be more tender and fall off the bone.

Call me a pervert but I actually prefer skimmed milk to full fat. OTOH low fat butter or cheese is an ABOMINATION.

How were adverse effects reported apart from simply asking participants? How would they know to report higher higher fasting glucose levels if not tested but otherwise symptom-free? Same goes for lower coQ10 or increased visceral/arterial calcification and any other adverse effects which at least in the early stages may not be visible. “I feel fine, Doctor.” Perhaps you aren’t.

John
My lipids doctor assured me that CoQ10 had no effect since there was no reliable research that proved it. He went on to define reliable as being in a top class review New England Journal etc, and number of citations.
On that basis rapid change or diffusion of new knowledge is going to rather slow.

Mr Chris
The man has an absence of any knowledge and is simply displaying his brainwashing, bias and stupidity.
Does he not know that Merck has two patents combining CoQ10 with each of their two statins?
Does he not know that Dr Peter Langsjoens who has several research papers on the subject? (check Pubmed for the name)
An interesting example is:Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms.
Okuyama H, Langsjoen PH, Hamazaki T, Ogushi Y, Hama R, Kobayashi T, Uchino H.
Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms.
Expert Rev Clin Pharmacol. 2015 Mar;8(2):189-99.
PMID: 25655639Abstract
In contrast to the current belief that cholesterol reduction with statins decreases atherosclerosis, we present a perspective that statins may be causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels through the depletion of coenzyme Q10 and ‘heme A’, and thereby ATP generation. Statins inhibit the synthesis of vitamin K2, the cofactor for matrix Gla-protein activation, which in turn protects arteries from calcification. Statins inhibit the biosynthesis of selenium containing proteins, one of which is glutathione peroxidase serving to suppress peroxidative stress. An impairment of selenoprotein biosynthesis may be a factor in congestive heart failure, reminiscent of the dilated cardiomyopathies seen with selenium deficiency. Thus, the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically reevaluated.
KEYWORDS:
ATP generation; atherosclerosis; coenzyme Q10; heart failure; mitochondrial toxin; selenoprotein; statin; statin cardiomyopathy; vitamin K2

Mike, that’s an interesting link, but I need to spend $59 to read the document. I note there is a comment on the pubmed page by John Tucker who suggests the paper won’t carry much weight against the phase 3 trials which involved tens of thousands of people. Would these have been pharma sponsored trials conducted with the usual deception tactics employed?

Thanks Mr. Chris & Mike—-I mention C0Q10 to every person I happen to encounter who is taking statins—-I don’t remember one person saying their MD already suggested that they supplement with CoQ10——

FIRST DRUG TO IMPROVE HEART FAILURE MORTALITY IN OVER A DECADE

Coenzyme Q10 decreases all cause mortality by half in randomised double blind trial
CoQ10 is the first medication to improve survival in chronic heart failure since ACE inhibitors and beta blockers more than a decade ago and should be added to standard heart failure therapy.

Lisbon, 25 May 2013: Coenzyme Q10 decreases all cause mortality by half, according to the results of a multicentre randomised double blind trial presented today at Heart Failure 2013 congress. It is the first drug to improve heart failure mortality in over a decade and should be added to standard treatment, according to lead author Professor Svend Aage Mortensen (Copenhagen, Denmark).

Heart Failure 2013 is being held from 25-28 May in Lisbon, Portugal. It is the main annual meeting of the Heart Failure Association of the European Society of Cardiology (1).
Coenzyme Q10 (CoQ10) occurs naturally in the body and is essential to survival. CoQ10 works as an electron carrier in the mitochondria, the powerhouse of the cells, to produce energy and is also a powerful antioxidant. It is the only antioxidant that humans synthesise in the body.
CoQ10 levels are decreased in the heart muscle of patients with heart failure, with the deficiency becoming more pronounced as heart failure severity worsens. Statins are used to treat many patients with heart failure because they block the synthesis of cholesterol, but these drugs also block the synthesis of CoQ10, which further decreases levels in the body.

Double blind controlled trials have shown that CoQ10 improves symptoms, functional capacity and quality of life in patients with heart failure with no side effects. But until now, no trials have been statistically powered to address effects on survival.

The Q-SYMBIO study (2) randomised 420 patients with severe heart failure (New York Heart Association (NYHA) Class III or IV) to CoQ10 or placebo and followed them for 2 years. The primary endpoint was time to first major adverse cardiovascular event (MACE) which included unplanned hospitalisation due to worsening of heart failure, cardiovascular death, urgent cardiac transplantation and mechanical circulatory support. Participating centres were in Denmark, Sweden, Austria, Slovakia, Poland, Hungary, India, Malaysia and Australia.

CoQ10 halved the risk of MACE, with 29 (14%) patients in the CoQ10 group reaching the primary endpoint compared to 55 (25%) patients in the placebo group (hazard ratio=2; p=0.003). CoQ10 also halved the risk of dying from all causes, which occurred in 18 (9%) patients in the CoQ10 group compared to 36 (17%) patients in the placebo group (hazard ratio=2.1; p=0.01).
CoQ10 treated patients had significantly lower cardiovascular mortality (p=0,02) and lower occurrence of hospitalisations for heart failure (p=0.05). There were fewer adverse events in the CoQ10 group compared to the placebo group (p=0.073).

Professor Mortensen said: “CoQ10 is the first medication to improve survival in chronic heart failure since ACE inhibitors and beta blockers more than a decade ago and should be added to standard heart failure therapy.”

He added: “Other heart failure medications block rather than enhance cellular processes and may have side effects. Supplementation with CoQ10, which is a natural and safe substance, corrects a deficiency in the body and blocks the vicious metabolic cycle in chronic heart failure called the energy starved heart.”
CoQ10 is present in food, including red meat, plants and fish, but levels are insufficient to impact on heart failure. CoQ10 is also sold over the counter as a food supplement but Professor Mortensen said: “Food supplements can influence the effect of other medications including anticoagulants and patients should seek advice from their doctor before taking them.”
Patients with ischaemic heart disease who use statins could also benefit from CoQ10 supplementation.

Authors
ESC Press Officepress@escardio.org
Office: +334 92 94 77 56
On Site contact: +3 51 916 30 63 49
About the European Society of Cardiology (ESC)
The European Society of Cardiology (ESC) represents more than 80,000 cardiology professionals across Europe and the Mediterranean. Its mission is to reduce the burden of cardiovascular disease in Europe.
About the Heart Failure Association (HFA)
The Heart Failure Association (HFA) is a registered branch of the ESC. Its aim is to improve quality of life and longevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
For practical information about heart failure aimed at patients, families and caregivers, visit the HFA’s Heart Failure Matters website.
About press registration
On-site registration opens 25 May 2013 in Lisbon supported by presentation of a press card or letter of assignment with proof of 3 published articles together with the filled in and signed embargo form 2013.
Scientific Programme Online
References

Heart Failure 2013
SA Mortensen, A Kumar, P Dolliner, et al. The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure. Results from the Q-SYMBIO study. Presented at Heart Failure Congress 2013 Final Programme Number 440.
The full title of the Q-SYMBIO study is: “Coenzyme Q10 as adjunctive treatment of chronic heart failure: a randomised double blind multicentre trial with focus on changes in symptoms, biomarker status with BNP and long term outcome”

Errett: Seven years ago our GP prescribed 20mg Lovaststin for my wife, with a post-it note attached for 100-200mg CoQ10. She never filled the prescription, as I have conducted a household propaganda campaign against them for a very long time.

To all
As Dr Graveline has pointed out statins also interfere with the seleno-proteins (anti-oxidants) and the dolichols which are in turn associated with glycoproteins. To quote:Our hormones of emotion, commonly known as neuropeptides, are just one small part of what glycoproteins do. They also are vital for cell identification, messaging and immunodefense.https://spacedoc.com/articles/dolichols-personality-change-and-statins

The dose used in this ‘trial’, 10mg is probably tolerated by quite a lot, if not most, participants. I believe with statins, based on my personal experience that this is a perfect case of ‘poison is in the dose’ . I think that even 10mg/day over time will cause problems but given that people are using 20, 40, even 80mg/day the likelihood of the well documented side effects is radically increased. Perhaps the creators of this ‘study’ would like to extend their work into side effects in relation to statin dosage.

Did the astroturfer Sever ever consider a genetic factor in relation to his “nocebo”effects?
Did not find any of the following refs in his “research paper”. I really begin to consider any medical study on drugs and supported by Big Pharma is not worth the paper it is written on unless the full data set is open to independent examination. This clearly not the case with any of the “so-called research” emanating from the Sever-Collins clique.

I suspect that if this lot even knew about the following studies, they simply ignored them in typical statinist style

This nocebo idea seems flawed to me, as I understand it the idea is that you experience bad side effects more if you know that a drug may cause them. There are other factors at play

Firstly, this is partly true, some people will believe that they have been affected by a drug. Isn’t this human nature.

However, more importantly, you may realise on becoming aware of side effects that indeed this has been the origin of problem. It’s called putting two and two together, humans have been doing this since the dawn of time. The statin effects are particularly insidious as they can be so easily dismissed as just being down to age and I believe the ASCOT group are older men so things like insomnia, muscle weakness can be rationalised as just the ageing process. A man of 64 saying that he’s not as fit as he once was is accepted as just getting older by both patient and doctor.

Also, the dosage of statins, 10mg bd is low is it not. What happens at higher dosage levels?

Re Side Effects:
I was in the A&E dept of a major London hospital a few back and I had the following exchange with the doc who was handling my case, who asked me if I was allergic to anything? I said yes, I was allergic to bisoprol fumarate (I think it’s some kind of beta blocker) and she corrected me and said, ‘No, you’re not allergic to it, you had an adverse reaction.’

What happens at higher dosage levels? …Well, if you are me, and you are taking 80mgs of Atorvastatin for about 5 weeks, your LFT’s rise up to 1300 instead of about 56, and you are rushed into hospital to see why….Of course, it’s nothing to do with the “adverse effects” of statins, it’s because you must have gallstones! How could this amazing, life saving, wonder drug be to blame? By the way, as for experiencing bad side effects because you are expecting them…shame on me, I hadn’t even heard of statins, nor knew anyone who took them. Now of course I know everyone and his grannie are on them(but not me!) 👍🏻

I guess that we by definition must have different sensitivities to “everything” including such things as the obvious “poison” which the statins constitute.

My wife, being interested in her genetic connections with other people, has taken a standard gene test (23 and me) and has among many other things been categorically warned about taking any statins so there seems to be “knowledge” around.

Goran
I too have had my “genes” checked by 23andme. Well worth it. Unfortunately nothing about stattin intolerance despite problems in that area. But definitely associated with Northern Europe and a high neanderthal association.
I bought a multi-garden tool but can’t use it thanks to statins – loss of muscle power – mentioned it to a previous GP but unwisely suggested it might be I was getting old.

Mark
Thanks for the link.
I note with interest that while the LDL reduction is listed, the actual effect on the incidence of new onset CVD/CHD/CAD is conveniently ignored along with “saved lives”
This is what I call astroturfing and agnotologizing of the worst kind. A serious example of the sin of ommission

Mike
Thanks for the link
I was on Crestor 5mg alternate days. See thats its very stong, no wonder combined with Ezetrol I had problems. Interesting thing is my lipidist didn’t put them down to lack of cholesterol.

Wow. You all must get your password and read this stuff.
“Debate on LDL Role in Heart Disease Reignited Out of the Blue”http://www.medscape.com/viewarticle/879731
The comments are particularly heated and opinionated. Sample:

Dr. Gregory Sloop
May 10, 2017

Kudos to anyone who recognizes that LDL is not the “cause” of atherothrombosis and calls for a paradigm shift. The authors are correct: saturated fats do not clog arteries. Thrombus does. Coronary artery disease is caused by increased blood viscosity which fosters mural thrombosis. Organization of mural thrombi leads to development of an atherosclerotic plaque as the thrombus undergoes neovascularization, allowing influx of myofibroblasts which synthesize collagen. The unsaturated fats in the Mediterranean diet and omega-3 fatty acids have bent carbon chains which prevents their tight packing in the erythrocyte plasma membrane, increasing its fluidity and erythrocyte deformability. This decreases blood viscosity. Long-chain saturated fatty acids and trans fatty acids have straight carbon chains, allowing close packing in the erythrocyte plasma membrane, increasing van der Waals interactions, decreasing membrane fluidity and deformability and raising blood viscosity. Removal of trans fats from the diet decreases blood viscosity, which is reflected in rapidly decreased cardiac death rates as seen in Denmark and certain counties in New York state. LDL increases blood viscosity by increasing erythrocyte aggregation. HDL decreases blood viscosity by antagonizing LDL binding to erythrocytes. All true risk factors for atherothrombosis, including age, male gender, hypertension, obesity, metabolic syndrome, cigarette smoking, increased hematocrit, and hyperfibrinogenemia are associated with increased blood viscosity. Thus, the cause of atherothrombosis is the organized mural thrombus, a non-specific lesion which is the end result of a common, nonspecific abnormality. The same process leads to superimposed thrombosis, the cause of most symptomatic disease. Yes, it is time for a paradigm shift. See Blood Viscosity: Its Role in Cardiovascular Pathophysiology and Hematology from Nova Biomedical Publishing if this topic is of interest..

Who is this Greg Sloop fellah? He certainly holds his own throughout the comments.

I thought so too.
To have referenced membrane potentials and the physics of colloids could have lent extra Kudos to a thought provoking comment about viscosity.
To have referenced membrane potentials in a discussion about thromogenesis necessitating some variation to membrane potentials could have cast added light from an additional angle.
To have mentioned that antioxidants help combat attrition of and compromise to membrane potentials (oxidative stress) thus maintaining them and thus combating rises in viscosity may have bundled the package more securely.
Those affairs which go on in blood are bound by the natural laws of physics. Rarely is the colloidal nature of blood adequately explored, explained, or otherwise referenced in discussions given over to the affairs of blood.

Had a look at the comments . . . It was encouraging that a significant number of the responses were not supportive of the European Atherosclerosis Society Consensus Panel’s consensus. Many people pointed out the conflict of interest of the main author: Ference . . . “research grants from Merck, Amgen and Esperion Therapeutics and received honoraria for lectures, consulting and/or advisory board membership from Merck, Amgen, Esperion, Ionis, and the American College of Cardiology.

Most of the other authors have a similarly comprehensive list of conflict of interest entries.

One of the signals that a group, feeling that the intellectual foundation of their beliefs is being threatened, is to invoke, like a defensive shield wall, the ‘Consensus’. This is an attempt to stifle debate that might undermine their certainties. I always know I am on the right side of an argument when the other side invokes the “Consensus”.

I only skimmed the ‘Consensus’ document . . . and I have to admit I did not see the other hallmark of the weak science/scientist . . . Proclaiming: “This is *settle* science” . . . “so what is there to discuss?”, However, they did have a pop at the ‘deniers’ who continued to deny even in the face of such overwhelming evidence – 200 studies and 20 million people . . . Wow! 200 sow’s ears . . . do we now have a silk purse?

The most impressing part of the list is to me that each entry has a plausible “explanation” to why a specific adversity occurs.

But I am always getting so very confused by the incredible complexity involved in each step our physiology, a fact which also makes me almost allergic to categorical statements. So my lingering question is if we could say anything about how strong these associations are?

In the name of the wee man…….!!! Thank goodness we have you to read all of this stuff for us and give us the truth. I couldn’t walk on statins and I don’t read the side effects part of medical leaflets. How did my brain know?

The Conservative Party is promising to provide a ‘free’ school breakfast at primary school. Existing breakfasts consist of cereals with low-fat milk, toast and fruit. That should create plenty of patients for the diabetes industry, who will then tell them to eat plenty of carbs.

Malcolm, Attached is a panoramic photo showing cholesterol biosynthesis. HMG CoA reductase is highlighted in yellow at far left. Look at all the cofactors, hormones, and vitamins that are downstream! This class of drugs cannot be good for us, based on this alone. Photo is of a poster “Biochemical Pathways” put out by Boehringer Mannheim GMBH in 1976. I’ve kept this since medical school. Thought you might find it useful for a future blog post. Discussion on the latest post has been amazing!

Keep up the great work!

Richard On Thu, May 25, 2017 at 12:18 Dr. Malcolm Kendrick wrote:

> Stephen T commented: “The Conservative Party is promising to provide a > ‘free’ school breakfast at primary school. Existing breakfasts consist of > cereals with low-fat milk, toast and fruit. That should create plenty of > patients for the diabetes industry, who will then tell th” >

I heard about those “nutritious breakfasts” too. Neither nutritious nor breakfast. The interviewee said without breakfasts children become in attentive and disruptive. What is that junk food going to do for them? They will have glyphosate contaminated wheat product, probably with added sugar, followed by denatured and denutrified milk, followed by more glyphosate contaminated product, followed by some fruit. It would depend which fruit but it is possibly ok. If they wanted nutrition, scrambled egg would be a better choice.

Yup! So that’ll be cereal, low fat milk, toast with “healthy low fat spread”, and fruit for breakfast; sandwich, fruit and oreos for lunch; biscuits for tea; and pizza or pasta for supper. Fruit juice or pop to drink. They should all be needing diabetes medication before they’re thirty, and statins before they’re forty, while being castigated for being couch potatoes snacking on crisps and popcorn every evening…

Disgraceful but not specifically a Tory party but a Dept of Health and medical establishment contribution. In short by experts who should know better but are following Big Pharma ambitions to treat everyone – ill or currently in good health.
Dr JR Kraft Diabetes and you
Dr Kraft puts hyperinsulinaemia at the top of the factors causing CVD, CHD and CAD and has a wealth of hard data to support his thesis

A set of lectures by Ivor Cummins
Ivor Cummins is an Irish engineer. It is interesting to see that an engineer seems able to understand the problems of hyperinsulinaemia and cholesterolaemia far better than medical experts in their specialty. There must be some reason – may I suggest money and status

There are some great lectures on diabetes, hyperinsulinieamia, heart disease and their interactions. The problem lies so much in “medical dogmas” that seem to be more directed at maintaining Big Pharma profits and the KOLs status and reputation.

Without triglycerides your liver would rapidly fill up with fat and you would die of NASH (non-alcoholic steotohepatitis). The best way to lower serum triglycerides is to eat a high fat, low carb diet. The body can store around 1.500Kcal of carbohydrate, primarily as glycogen. The liver stores about 500Kcal. Once these stores are full, any further carbohydrate/glucose will be converted to fat in the liver – then transported out via triglycerides aka VLDL. VLDL will then transfer the fat to fat cells around the body, shrink down to LDL, at which point the LDL will mostly be reabsorbed back into the liver. In short, triglycerides have a critical function in protecting the liver from destruction if you eat too many carbs.

Whenever people start talking about triglycerides, I get an uneasy sense of confusion because here is a definition of these beasts:

“A triglyceride is an ester derived from glycerol and three fatty acids. Triglycerides are the main constituents of body fat in humans and other animals, as well as vegetable fat.”

In other words, triglycerides is just a fancy name for fat. Butter and cheese are huge blocks of triglycerides!

So given that, triglycerides seem to enter medicine thus:

1) Saturated triglycerides have traditionally been a bogey man as far as heart disease is concerned. However, new thinking exonerates saturates triglycerides in food!

2) Unsaturated (cis) triglycerides are OK according to conventional ideas, but multiply unsaturated (cis) triglycerides are not according to new thinking.

3) Unsaturated trans triglycerides get a universal thumbs down.

4) Meanwhile it would seem that the liver accumulates triglycerides if people eat less triglycerides!

5) Everyone seems to agree that triglycerides in the blood is a very bad sign as far as heart disease is concerned.

Obviously the use of two terms for essentially the same thing has intensified this confusion. As a layman in these matters, I think I could make a stab at unravelling some of the above paradoxes, but I would really appreciate some heavy-duty clarification – maybe even a whole blog post devoted to this! Or have I just made some fundamental blunder (my chemistry degree was over 40 years ago).

David. You are right to be confused. A triglyceride is one glycerol molecule attached to three fatty acids. The chemical structure of a triglyceride.

However, for reasons unknown, the lipoprotein called a Very Low Density Lipoprotein (VLDL) is also called a triglyceride. This is very confusing, perhaps deliberately so? Anyway, when people talk about triglyceride levels, they mean VLDL levels. Just as when people talk about cholesterol levels they do not mean cholesterol levels, they mean a combination of LDL, HDL and a percentage of the VLDL level.

Dr. Kendrick: Thank you for the clarification. It appears that VLDL is calculated by dividing triglycerides by 5, which I suppose means that there are on average about five of the little rascals carried by each lipoprotein as they wend their way through the bloodstream delivering them, at the time when they are measured.

Gary, I have long since given up trying to work out what ‘cholesterol’ levels mean. We have now moved on to LDL-C to LDL-P, light and fluffy LDL to small and dense LDL. We have good cholesterol, bad cholesterol, good bad cholesterol and bad good cholesterol. I don’t think any other possibilities exist. Perhaps we shall end up with Schrodinger’s cholesterol. We won’t know if it is good, or bad, until we open the box and observe what has happened. ‘Its quantum LDL, baby.’

Thanks for that! Just to push you a bit further, do the tests for triglycerides actually measure just VLDL or are they also sensitive to fat in the blood (obviously fat would not dissolve, but it could be present in colloidal suspension I suppose)

Maybe it would help to always write” triglycerides (VLDL)” just in case there are others as confused as I was!

Oh.
Thank you doc. I might have put that together myself if I’d searched a bit harder, but I’d never heard of “triglycerides'” useful function from anywhere. Is it knowledge that’s so common it’s never spoken of?

Are the genetically interesting people in the above article at risk for fatty liver?

May I plead with you all to keep a watch on the BMJ and to use their RAPID RESPONSE system just as one uses Dr Kendrick’s comment section. Many of the comments and references cited here are equally valid on some relevant editorials, news items and even reports. All one has to do is give name and rough address and answer a question or two. Open to all including doctors.

May I take this opportunity to suggest that any one, a patient, carer and prticularly doctors as the ultimate carers sign up as “patient reviewers”. Interesting and gets patients and carers involved. Too long have patients been treated little better than pets (may be with less respect??). It is people like Dr Kendrick that have given patients an outlet to express their views and knowledge.

Yes, you’re right Mike.
I once had to have a test on my bladder that required me to stand with a tube inserted sending in water for about 15 minutes. I had a male and a female nurse either side of me and holding a conversation. I thought I would join in. They seemed put out. I persisted out of bloody mindedness. I refused to feel like some object between them.
Thought I have to say I had an operation for removing a possible cancer mole (wasn’t cancerous) and had a great time joking with the Iranian doctor carrying out the operation.
It’s not exactly what you are saying, Mike, but it is all part of the same mentality.

Mike Cawdrey. RIP. Posted above remark at 0941, May 26th. Later discovered savagely murdered at 1540 that same day. Shocked and speechless.

Save for the following:
Mike was so right about the BMJ. Where most medical science journals are far too conservative the BMJ has been a champion of that which is refreshingly progressive in the general stable of medical journalism and peer review. The BMJ has revealed proactive concern for the spread of poly-pharmacy (and other matters) and openly invites laypeople to participate in the process of peer review.
Please, if you have the time do engage with the BMJ do not be afraid to place remarks and comments beneath open articles. Sign up as a peer reviewer, start reading articles, and do so even if you do not feel sufficiently knowledgeable or competent. There is no compunction to review anything. Having said that some articles are so appealingly conceived and so ill written that you may feel compelled to submit a critical review.
Whatever you choose do do honour the memory of this stalwart conviction campaigner whose life and activism was so brutally cut short.
For all the good that medicine, medical science, and medical practice has to offer, patients need not be the cash-cows they are taken for in the areas in need of so much improvement. Informed patients and engaged consumers must press home the point.
A paradigm shift is needed where medical science and practice has greater regard for health science (where health science is based upon a wholesome understanding of the things that maintain health and the departures from which hasten the trend to ill-health.
The day may come. Old and dogmatic ideas may fall. They sure as hell will fall quicker the more people (patients and consumers) bring pressure to bear from the ground up and take inspiration form the likes of Mike Cawdrey.

Well, Goutboy….there may be some minor, obscure benefits as mentioned in the paper, but at what cost? My life was miserable on statins; I developed Type 2, I had to give up driving due to severe shoulder pain, I started to walk slower and slower, etc.
No….any attributes of statins appear to have to be searched out, and not at all obvious.

Excerpt:
“They then developed a computer model that suggested vitamin D could be effectively synthesized at tropical rates across the entire globe for three quarters of the year and that the ability to synthesize it dropped off gradually between 40 and 70 degrees latitude during the winter months, and only regions between 70 and 90 degrees latitude had a complete vitamin D winter.”

Goutboy
Read the review. I am very sure he does not agree with much of the science. Seems to review the book for its humour, which I think is a mistake.
But, as my mother in law, used to say ” Does X know” ?
Having read the review , a bit of his site, I tend to stick with Dr. K

“However, for reasons unknown, the lipoprotein called a Very Low Density Lipoprotein (VLDL) is also called a triglyceride. This is very confusing, perhaps deliberately so? ”

Thinking about this, whatever mistake started this nonsense off, continuing this mistake simply has to be deliberate. I mean it is one thing to give a single word two meanings – particularly if they relate to completely different areas of science – but calling VLDL a triglyceride is at a different level, because the word triglyceride actually contains information about the structure of a fat molecule! It is rather like referring to washing soda (sodium carbonate) as sodium chloride!

I would guess a lot of people told by their doctors that they have a raised triglyceride level, have looked that up – discovered it meant fat – and gone on a low fat diet!

David,
Triglycerides are lipophiic and hydrophobic. If free triglycerides were transported in the blood they would form globules (like washing fat off a greasy saucepan), and block blood vessels.
VLDL covers the triglyceride in a layer of cholesterol and lipoprotein which is hydrophobic/ lipophilic on the inside and hydrophilic/ lipobhobic on the outside.
The liver makes VLDL particles to encapsulate the triglycerides and allow them to be transported to the periphery without jamming up blood vessels.
VLDL is an analog for triglyceride, once you have subtracted the lipoprotein and cholesterol ( I cant remember quite which but it is either triglyceride or VLDL which is easier to measure, an the other one is back calculated from the one measured.

IMO my GP’s knowledge has advanced a lot over the years, but she is still convinced that dietary fat is the only reason for blood fats, including triglycerides. An interesting study by Richard Feinman et al. shows that free fatty acids in the blood relate directly to carbohydrate consumption – when the body is overloaded with glucose it processes it as fast as possible to get it out of the way before it starts glycating everything, and leaves the fats until later. Of course if you then eat MOAR CARBS like the dietician says, later never comes.

I’m very confused by this – partly because trying to find the original study paper defeated me, and I got lost in the labyrinthine links, trying to track down who’d actually put up the money for the study that appeared to show that statins helped prevent cardiomyopathy (if that’s the correct term). It takes hours burrowing around identifying where the money is actually coming from….it all sounds dodgy to me. But one thought, probably completely scientifically off the wall – if the authors are arguing that statins have an improving effect on heart muscle – then surely they are acknowledging that statins do have an effect on muscle function? Unless heart muscle is totally different?

@Dr. William Feeman Unfortunately targeting lipids is a dead end research. If manufactures care about the profits they should abandon this target. There is already enough evidence that even after LDL-C drop to 30mg/dL by statins +/- ezetimibe and PCSK9 inhibition “residual” CV risk remains. Lipid lowering in addition to statins when used along with aspirin or DAPT, b-blockers, ACEi or ARB’s, coronary revascularization for “stable” and not so stable CHD didn’t reduce mortality as both IMPROVE-IT in almost 7 years and FOURIER in just over 2 years have shown.
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Dr. William Feeman| Family Medicine
3 days ago

@Dr. Alexei Chataline @Dr. William Feeman The Cholesterol Crusade is alive and well!!! You should know the history of atherothrombotic disease (ATD) quite well, but just to refresh your memory: Populations with chronic low lipid (LDL-cholesterol) levels rarely have ATD, or at least not until old age. People with genetic mutations resulting in low lipid levels likewise rarely get ATD. People with dyslipidemia do get ATD events, and adequate correction of dyslipidemia results in regression of plaque. LDL-cholesterol can be seen entering the artery wall and HDL cholesterol can be seen exiting the artery wall. Where is the problem?
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So, who is this Dr Feeman when he’s at home? Pops up in many comment venues.

Much of the research I’ve read leads me to believe that biochemistry is actually a stack of superimposed U curves and J curves. Only the drug companies portray things as purely linear, after all they have drugs to lower or raise things and this paradigm leads to increased sales.

Marika at FOODMED.NET has posted an article about salt. Since sodium and potassium are partners at the dance, I think it worthwhile to purchase the book she discusses, “The Salt Fix,” by Dr. James DiNicolantino. He is pro-salt, by the way.

Mr Chris. John’s synopsis of Dr K’s contributions over all this time does seem disingenuous, but I agree with his analysis of the state of the NHS, and the over prescribing of so many medicines, which he, and I, and others on this blog, have shown to be detrimental to our health. Many bloggers explain that they feel better without the toxic combinations doled out from their NHS surgeries…..frequently at the behest of the Practice Nurse, who apparently reads a computer screen, which interprets blood results according to accepted norms, as laid down by computer programmers. (are there medics behind such regimes?), then voila! Out pops a printed prescription.
As a retired Registered Nurse, it annoys me to see the way Nursing has ‘developed’ over the last 15 years, and I feel the role of the Patient Advocate has been lost. Who is there to speak up for the patient, who cannot be expected to understand such things?

Dr Kendrick cannot provide individual patient advice over the Internet. UK General Medical Council regulations are clear that to do so would be a breach of medical standards that could result in disciplinary proceedings.

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